Biology 121 – Lectures 1-8 – Unit 1

Lectures 1-2
A) How Many
 1.9 million species
o 950,00 insects

o 60,00 vertebrates

o 380,000 plants

 Total Diversity: 8.7 million species

 1/2 species 6% land tropical forests 9fire)
 Losing species (genetic diversity)
Biological diversity
1. Self-interest / greed
2. free market environmentalism
3. Ethical approach
B) Clarify life
 Taxonomy - maximizing / clarifying
 Systematics - evolution / genetic relationships - tree of life
 Kingdom, phylum, class, order, family, genius, species
o King Philip's came over for great sex (lol)

2. Kingdom:
 The highest and broadest level of classification.
 There are traditionally five kingdoms: Animalia (animals), Plantae
(plants), Fungi (fungi), Protista (mostly single-celled organisms), and
Monera (bacteria, which is now often divided into Bacteria and Archaea).
3. Phylum:
 A major category within a kingdom.
  Organisms within a phylum share a basic structural framework. For
example, the phylum Chordata includes all animals with a notochord, such
as vertebrates.
4. Class:
 A category within a phylum.
 Classes group organisms that share more specific similarities. For
example, the class Mammalia includes all mammals, characterized by
features like having hair and mammary glands.
5. Order:
 A category within a class.
 Orders group organisms that are even more closely related. For instance,
the order Carnivora includes carnivorous mammals like lions and bears.
6. Family:
 A category within an order.
 Families group organisms that share a very close common ancestry. For
example, the family Felidae includes all cats, from domestic cats to lions
and tigers.
7. Genus:
 A category within a family.
 Genera (plural of genus) group species that are very closely related. For
example, the genus Panthera includes lions, tigers, leopards, and jaguars.
8. Species:
 The most specific level of classification.
 A species consists of individuals that can interbreed and produce fertile
offspring. For instance, the species name for the domestic cat is Felis
catus.
 Phylogenetic tree - graphical representation of the evolutionary relationships
C) Molecular Phylogeny
 Proteins / nucleic acids
o Proteins - amino acids differences (common ancestor)
 o Which molecule?

1. Universally distributed
2. Functionally similar
3. Homologous parts - parts of the molecule should be exactly the same
4. Change in rate that is commensurate with evolution distance measured
1. broader the distance = slower the rate of change
1. Cytochrome C - slowly evolving → phylogenetic tree
2. DNA - nucleotide change more rapidly - recent splits of
lineages
3. **490-91
D) The 5 Kingdoms
1. Cell structure
2. mutation
3.
1. Moena - bacteria - prokaryote - unicellular
2. Plans - eukaryotic “protozons”
3. Plants - PHS (all have cellulose cell walls)
4. Fungai -
1. decompose
2. chitin cell wall
5. Animals - particulate food, no cell wall
4. Prokaryote VS Eukaryote p529-71
5. Asexual reproduction
6. no organelles
7. circle chromosomes
sex/asexual
yes
no
E) 6 Kingdoms
Sequence ribosomal RNA
Monera → archaebacteria - challenging environments
→ eubacteria
F) 3 Domains?
 Woese - Ribosomal RNA
o Universally distributed

o Functionally constant (does the same thing for everyone (makes DNA in the
body))
o Homologous parts

o Slowly

 Bacteria / Archaea / Eucharia

G) Requirements for life
1. Metabolism - storage / use of chemical energy
2. Reproduction - continuation of form over time
3. Genetics - pass information (from one generation to the next)
4. Evolution - ability to change
5. Growth - how it changes over time
6. Adaptation - respond to the environment
H) Solutions
1. Common (unity of life)
1. replicate DNA
2. major metabolic pathways (glycolysis - energy)
3. Genetic code
2. Different - Climate too stressful
1. bacteria / fungi → spores
 2. plants → seeds / go dormant
3. Animals → hibernate / migrate
4. Protista → cysts
I) Nutrient
1. Atrophy - synthesis organic rich compounds from INORGANIC sources
2. Photoautotrophs - plants, light energy source
1. Chemo auto trophy - Sulfur / CO2 gets energy H2
2. H2+S → H2S + energy
3. Co2+ 4H2 → CH4 +2H2O + energy
2. Heterotrophy Chemotrophs 544-45
energy from organic sources
1. Predation
2. Parasitism
3. Detritovore - unitize waste products
3. Mixotrophy - both organic and inorganic sources
Carnivores plants PHS / interact - nitrogen
 Microalga - PHS / ingest prey by photogenic
 golden alfa - voracious predators

LECTURE 3
A. Biological Molecules

 Made up of carbon, hydrogen, and oxygen and nitrogen and

 They are polymers (monomers) - Universe

 Variation in sequence

 100 amino acid sequences

o 20 X 10^100 = 10^130

 Cell is about 70% water

 B. Carbohydrates

 Carbon

 Hydrogen

 Oxygen

 2:1 ratio CH2O

Functions

o Energy – glucose

o Stored energy

o Structural components

 cellulose – plants

 chitin – fungi exoskeletons

2. Monosaccharides

 3c – triser – glyceraldehyde C3H6O3

 5c – pentoses – ribose C5H10O5 deoxyribose C5H10O4

 6c – hexose – glycose C6O6H6

o Disaccharides -double oxygen

o Sucrose – glucose + fructose

 Dehydration reaction – lose H2O

4) Polysaccharides

o Starch – easily depleted (lots of glucoses)

o Cellulose – unbranched structure – stable (lots of glucoses)

 Cotton is 90% cellulose

o Chitin – nitrogen amino sugar (P58)

 Lipids – C-H-O but not 2:1 ratio (not polymers)

o Insoluble in H2O

 Functions

o Membrane structure (phospholipids)

o Energy storage

 2.5 g, 2.0 g fat, 5.0 g glycose

 Mormaer / vitamins

 Triglycerides – fat – solid; oil – liquid

o Glycerol + 3 fatty acids

 Saturated fatty acids – max # H à pack together tightly

o Ex: animal fat

 Unsaturated fatty acids – doubled bonds à kinky à oils

 Cholesterol à from saturated fatty acids by liver

o Transported by LIPIDPROTEINS

 LDL (low density lipid protein) à deliver cholesterol to cells

 Delivery truck

 HDL (high density lipid protein) à take cholesterol to liver to be

degraded

 Garbage truck

 Cells laniary artery to heart à plaque, calcium, clog

 Leads to a heart attack

o Marie Daley –

o HDL – work agential procerus

o Pfizer – drug for HDL

 Low HDL levels associate with hear disease does not cause

 **correlation not causation

 High HDL à heart attacks

 Regular exercise LOWERS LDL

 Smoking raises plaque

 Butter/cheese raises LDL

 Total cholesterol in a person to be UNDER 200

  Cholesterol ratio = total cholesterol / HDL #

o Average:

 5 for men

 4.4 for women

 LDL under 100

 Statins à drugs that lower LDL

3) Phospholipids

o 2 fatty acids and phosphate group – glycerol

o Hydrophilic on one end (water)

o Hydrophobic on one end (no water)

o Membrane structure

4) steroid – 4 fused carbon rings

o testosterone

o Use steroids to build muscle -> big risks!

C. Proteins

a. Escherichia coli – 600-800 proteins

b. Humans 22,000 genes -> thousands of proteins

c. C-H-O-N sometimes P, S, Fe, Mg

d. 20 amino acids (P47)

e. Peptide bond -> condensation reaction (P45)

1. Function
 a. Support - ex: Collagen

b. Transport – ex: hemoglobin

c. Movement – ex: actin/myosin

d. Defense – ex: antibodies

e. Enzymatic – ex: speed up reactions

i. Amylase

ii. Lactose

2. Protein structure – critical for function

a. Primary – sequence of amino acids – polypeptide

b. Secondary – localized twisting/folding – alpha helix

c. Tertiary – folding due to interactions between R groups

i. H-S-S-H

d. Quaternary – several polypeptide chains

i. Changes in PH or changes in temperature -> protein denature

3. Enzymes – protein change rate of reaction

a. Small amounts

b. Catalysts

c. Specific

d. Lower energy of activation

e. Do not change free energy, change G

E) Nucleic Acids

o C-H-O-N-P

o Polymers of nucleotides – 3 parts

 1. Nitrogen base – purine (A/G)

 2. Sugar -

 3. Phosphate group

1. Function
 a. Information transfer

b. Synthesis of proteins

i. Beta-globin -> 441 (nucleotides in DNA) ; 147 RNA words ; 147 amino
acids

c. Chemical energy transfer

i. ATP = Adenine triphosphate

d. RNA – enzymes (ribozymes) regulate protein expression

2. DNA (deoxyribonucleic acid) VS RNA (Ribonucleic Acids

DNA (deoxyribonucleic RNA (Ribonucleic Acids

acid)

Sugar Deoxyribose Ribose

Bases A, G, C, T A, G, C, U

Strands Double Single

Compound Class of Monomer(s) Function

Compound

Collagen Protein Amino Acid Cell Structure

Glucose Carbohydrate Monosaccharide Energy Source

Hemoglobin Protein Amino Acid Oxygen
transport

DNA Nucleic Acid Nucleotide Genetic info

storage

Cholesterol Lipid Steroid (not a Membrane

polymer) Structure,
Precursor to
Hormones

RuBP Protein (Enzyme) Amino Acid Catalyzes Carbon

carboxylase Fixation in
Photosynthesis

Phospholipid Lipid Glycerol, Fatty Cell Membrane

Acids, Phosphate Structure
Group

Ribonucleic acid Nucleic Acid Nucleotde Protein synthesis,

Genetic
information
transfer

Starch Carbohydrate Glucose Energy storage in

plants
LECTURE 4
A) living is work

1. Order

2. Active transport

3. Membranes

4. Movement

5. Build complex molecules

6. Degrade molecule -> extract energy

B) Chemical energy

o ATP = Adenosine triphosphate

o Adenine + ribose + 3 phosphates

o ATP + H2O  ADP + Pi + 7.3 Kcal/mol

o Phosphorylation (regeneration of ATP)

o ADP + Pi + energy  ATP + H20

o Give phosphate  Protein (overall shape)

 Transporter proteins
C) How much

o Escherichia coli

o Poly saccharide – 2000 ATP

o Protein 1500 ATP

o DNA – 120000000 ATP

o Human – 10^25 ATP/day 1 billion ATP

D) How

o Regeneration

o C6H12)6 + 6O2 + H2) à 12H2O + 6CO2 + energy

E) How to burn glucose

o 1 mole glucose à 686 Kcal

o Oxidize glucose in small steps

o Redox - reduction / oxidation

o NAD = nicotinamide adenine dinucleotide

o NAD ox / NAD re

o NAD + / NAD H

 Oxidation = loss of electrons

 Reduction = gain of electrons

 LEO says GER

F) Overview of respiration

o 4 stages

1. Glycolysis

2. Oxidation – of pyruvate Acetyl COA

 a) Oxidation – loss of electrons

b) Reduction – gain of energy

c) Leo says Ger

3. Krebs citric acid cycle

4. Respiratory electron transport chain (ETC)

o NAD/ FAD à energy temporary storage

 Dump trucks

 NAD ox = empty dump truck

 NAD re = full dump truck

G) Glycolysis

 No oxygen needed

o Evolved early in the history of earth

o Happens in the cytosol (p175)

 Results:
 o 4 ATP – 2 ATP = 2 ATP rex

o 2 NAD re (NAD H)

 **Fermentation-

o Glycolysis + steps to regenerate NAD ox from NAD re (p 185)

 Fungi / bacteria 2 pyruvate + 2 NAD re  ethanol (2c) + NAD ox +

2CO2

 **Animal 2 pyruvate + 2 NAD re  2 lactic acid + 2 NAD ox

o 2 ATPP = 15 kcal / 686 kcal – 2%

I) Formation of Acetyl – CoA (Stage 2)

 Mitochondrion – matrix

o Pyruvate oxidation

J) Krebs citric acid cycle (Stage 3)

 2 acetol – CoA (2 carbon)

 Acetyl CoA + oxalacetate (4carbon) à citrate (6Carbon)

 Net (results)

o 4 CO2

o 2ATP
 o 6 NAD re

o 2 FAD re

 4 ATP generated directly

 Energy à10 NAD re 2 FAD re

K) Respiratory electron transport chain (stage 4)

 Transfer electrons à pathway of enzymes

 Last acceptor – O2  H2O

o Chemiosmotic gradient (p 181)

o Pump H+ across inner membrane

o Electrochemical gradient – charge / # of protons

o ATP leaves mitochondria (concentration of ATP is usually low)

  ATP synthase

 4 ATP

o NAD re – 2.5 ATP

o FAD re – 1.5 ATP

L) Final Energy Totals

M) Body heat

1. Cold blooded – poikilothermic / exothermic

2. Warm blooded – homeothermic / endothermic

a. Hair / feathers / fat / shiver

b. Cold temp we do well, hot places not too well

i. Hyperthermia (heat stroke)

Book Notes :

 Proteins are formed from different combinations of 20 amino acids, all

of which share chemical similarities

 Carbohydrates can form giant molecules by linking together chemically

similar sugar monomers (monosaccharides) to form polysaccharides
  Nucleic acids are formed from four kinds of nucleotides monomers
linked together in long chains

 Lipids also form large structures from a limited set of smaller

molecules, but in this case noncovalent forces maintain the
interactions between the lipid monomers that are held together by
covalent bonds

LECTURE 5
A) Life on Earth is Solar Powered
a. Photoautotrophic organisms  Light  chemical energy
i. PHS
b. CO2 + H2O (Light)  CH2O + O2
B) Historical Perspective 1850
1. C from CO2
2. N from soil
3. Light / chlorophyl  Increase dry weight
4. O2 goes up during the day … CO2 goes up at night
5. Both RSP (24/7) + PHS (light) ----- 4 and 5 go together
6. CO2 split  O2
i. Wrong
C) The Splitting of H2O
a. CO2 + 2H2S  CH2O +2S (yellow globs)
i. Plants split H2O (energy)  release O2
 ii. O18 isotope of oxygen
Experiment 1:
CO2 + 2H2O  CH2O + H20 + O2
Experiment 2:
CO2 + 2H2O  CH2O + H2O + O2
General equation for photosynthesis:
6CO2 + 12H20 + light Chlorophyl  C6H12O6 + 6O2 + 6H2O

D) The Two Stages of Photosynthesis

a. Light reaction – O2 produced -- energy
b. Dark reaction – does not need light directly (light independent)
i. CO2  CH2O
ii. Carbon dioxide is reduced
Algae – light  dark
(14)CO2
Light: 2H2O + light (Chlorophyl) O2 increases + 4[H+] + 4e-
Dark: CO2 + 4[H+] + 4e-  CH2O + H2O
ATP NADP re

E) Light and Chlorophyll

a. Proton – E – 1/l (wavelengths)
b. Pigments to absorb light  chlorophyll a
i. Absorption spectrum – Red-orange / blue wavelengths
ii. Acton spectrum – highest level of photosynthesis – red-orange / blue
F) Exciting an electron
a. Electron  higher energy level / unstable
b. Illuminate chlorophyll  floresces red
G) The Light reactions: Photophosphorylation

a. Non-cyclic  2 photosystems (p 200)

1. P680 – absorbs light
2. High energy electrons  primary electron acceptor (pheophytin)
3. Electrons are replaced by splitting H2O
4. Electron  photosystem II makes ATP
5. Fill ‘electron hole’ in P700
6. Electrons are passed y photosystem I  NADP ox  NADP re (NADPH)
H) The Dark reaction: Calvin Cycle

a. Fixation of carbon-

b.
 i. 6CO2 + 6 RUBP (ribose biphosphate 5C)  12 PGA phosplagricarate
(G3P)
ii. Rubisco (makes that reaction happen)
c. Reduction
i. 12 ATP + 12 NADP re
ii. Reduce PGA  xPGAL (3C)
1. Phospoglyceraldihyde
d. Regenerate RUBP
i. 6 RUMP (ribulose mono phosphate) + 6ATP  6RUBP
ii. 18 ATP + 12 NADP re  2 PGAL  1 glucose

I) C4 / CAM plants: Variation of a Theme (p205-208)

a. C3 +
b. C4 – structural separation of (fixation of CO2 + making sugar)
i. PEP (phosphofinal pyruvic acid) (3C)
ii. Fixes CO2 (from atmosphere)  C4 (exalactic)
iii. Transported to bundle sheet cells

iv. PEP + C02

 1. Pep carboxylase

v. Temp high intense light

1. Storage (creeping for gas exchange) close
a. [CO2] low [O2] high
2. O2 + RUBP  rubisco (photorespiration)
a. Wasteful
b. Produces no ATP
3. Uses fixed carbon
4. Photosynthesis rate goes down
vi. Pep carboxylase
1. Affinity 4[CO2] around rubisco (Calvin cycle)
vii. 2) CAM plants separation function + make sugar in time
viii. Stomata open at night for CO2 into C4
ix. PEP Carboxylase
c. C4 release CO2  RUBP (p 208)
d. Plant saves H2O
i. Found in desert plants, pineapple, etc

J) Metabolism – overview RSP PHS

a. H2O -----------------------------------------H2O
b. PHS RSP  carbon cycle (p1238-40)
 c. 10,000 years [CO2] stable, but since 1850 [CO2] increase
d. Increase in average temp

LECTURE 6 – Cellular Reproduction: Mitosis/Meiosis

A) Information transfer
a. DNA  MRNA  Proteins
b. Duplicated DNA 
B) Cell division
a. Linear / replicate / 1 copy  each cell
C) Mitosis – Eukaryotic Cell Division
1. Interphase –
1. DNA – chromosomes (nucleus)
2. Sister chromatids – centromere
3. Homologous chromosomes
2. Prophase
a. Humans – 23 pairs = 46 chromosomes
b. Pairs  diploid (2n)
c. No pair  haploid (n)
i. Eggs / sperm
d. Spindle fibers / nuclear membrane disappears
3. Metaphase
a. Two chromatids arranged on equatorial plate
b. Each chromosome behaves independently
4. Anaphase
a. Chromatids separate  poles
i. Chromosomes
5. Telophase
a. Cytokinesis – division of cytoplasm
 i. Results in 2 identical cells

D) Cell Cycle

i. Interphase G1, S, G2
b. Gap 1 – Chromosomes unreplicated
i. Regulatory nuclear – G1 checkpoint
c. Gap 0 – non dividing – terminally differentiated
d. S phase – Synthesis – genetic material replicates
i. 2 sister chromatids
e. Gap 2
f. M – Mitosis
E) Abnormal Cell Division = Cancer
a. Cancer – uncontrolled growth of cell
b. Multiple genetic mutations  in DNA cause cancer
c. Characteristics
1. Activate oncogenes – proteins – turned off
a) (mutated proteins) – jammed accelerator pedal
b) Kinase (turns on other proteins)
2. Tumor suppressor genes mutated – protein that inhibits cell division
a) Defective breaks
b) P53 gene – destroys defective cells – usually mutated (50% of
cancers)
 c) Replicative potential  immortal
a. Hela cells
b. Telomere – shortened in division -- regenerated in cancer
cells
d) Replicative potential  immortal
3. Replicative potential  immortal
a) Hela cells
b) Telomere – shortened in division- regenerated in cancer cells
4. Tumor angiogenesis  changing pathways for blood vessels
5. Metastasis – migrate in body
1. Virus – associated cancer
a. Human papilloma virus (HPV)  cervical cancer
b. Henrietta Lacas - Hela
2. Hereditary predisposition
a. Genes with mutations
b. Mutation BRCA-1 gene  50-80% chance of developing
breast cancer
1. Screen for cancer
2. Tamoxifen – prevents estrogen from binding
to cells
3. Provalactic mastectomy
a. Both breasts and ovaries
3. Carcinogens – exposer to air / water
a. 789 deaths – 36 died of lung cancer (smokers)
b. 150,000 cases of lung cancer annually – 96% smoke
cigarettes

F) Meiosis – reduction division (gives offspring half and half of DNA)

 a. 1 of each homologous chromosome  gametes
b. Only happens in:
i. Diploid cells
ii. reproductive tissues
1. Interphase I
a. make chemicals for different things
2. Prophase I
1. Homologous chromosomes – find and pair
2. Form tetrad (4 chromatids) together
i. 23 tetrads in humans
3. Crossing over – chromatids exchange pieces
3. Metaphase I
a. Tetrads line up
4. Anaphase I
a. Homologous chromosomes separate
5. Telophase I
a. Haploid nuclei form
i. ½ chromosomes
b. 2 chromatids – amount of DNA is the same as G1
c. Homologous pair oriented independently on plate

d.
 6. Interkinesis
a. no DNA replication
7. Prophase II
8. Metaphase II
a. chromatids not necessarily identical
9. Anaphase II
a. Chromatids go to opposite poles
i. Chromosomes
10. Telophase II
a. 4 new haploid cells

b.
G) Nondisjunction – Trisomy 21
a. Mistakes in miosis

b.
c. Trisomy—21 Down Syndrome – 3 copies of #21
d. 1-700 babies in US have Down Syndrome
e. 90% of the time it is an error in the egg
i. Results from woman’s age
f. Amniocentesis – amniotic fluid  karyotype
g. NIPT – noninvasive prenatal ternate – blood test
i. Fetal DNA
H) Comparison of Mitosis and Meiosis
Lecture 7

A) Life Comes Only from Life

B) Asexual Reproduction
1) Prokaryote - Binary Fission
a. Circular Chromosomes
b. No mitosis
2) Budding -- hydra
a. Dividing cells develop on parent, detach
3) Fragmentation – pieces  individual (p 892)
a. Algae / invertebrates (starfish)
4) Vegetative Reproduction – strawbenia – runners  cut / individuals
a. Pando – quaking aspen clone – 47000 trees
5) Parthenogenesis – unfertilized egg = haploid (male), diploid
(female)
a. P 893
C) Sexual Reproduction – 2 processes
a. 1. Meiosis – reproduction  haploid gametes
b. Syngamy (fertilization) – 2 gametes combine

c. One parent
d. Two parents
i. Diecious – vertebrates
e. More than two parents
i. 1/6 couples – airtid reproductive technologies (ART)
1. In Vitro Fertilization (IVF)
1. Egg fertilized in lab
 2. Louise Brown – born in 1978
3. IVF success rate depends on the mom
4. IVF success rate 10-25%
i. Under 35 – 40%
ii. Over 40 – 12%
2. Surrogate mothers –
1. $20,000 fee + $30-50,000 surrogate
2. Total cost -- $200,000
i. 5 “parent” – egg/sperm doner + birth
mom + individual parents
3. Clone – 5% success  deeper babies
f. Alternation of generations
i. Plant/Fungai Apollos (p182)
D) Levels of Genetic Variability
a. Asexual – mutations – low rate

PICTURE

1. Conjugation – transfer DNA large when joyed

2. Transformation – take up DNA from continent
3. Transduction – viruses transfer DNA
b. Sexual – mutation – low rate
i. 3 sources of genetic variation
1. Independent assortment of chromosomes
1. Metaphase 1 – homoeologous chromosomes
line up on plate
2. 2^n -- # of protatic combos n=haploid
number
3. 2^23 = about 8 million
2. Crossing over – prophase 1 (miosis)
1. Exchange genetic material
3. Random fertilization
1. Egg 1 in 8 million combinations
2. Sperm 1 in 8 million combinations
i. Zygote 1 in 64 trillion combos
E) Importance of Genetic Variability or Why Have Sex
a. Algae Protista claymates – both sex and associated
reproduction
i. Adults – haploid
ii. Asexual – mutations twice  4 adults
iii. Sexual – gamete cells (+/-)  diploid zygote
 1. Meiosis  haploid adults
iv. Possible stable environment  asexual
1. Unfavorable environmental conditions
b. Advantages vs. Disadvantages of Sex – producing genetically
diverse offspring
i. Adaptive variation
ii. Cost:
1. Reduce reproductive rate by ½
2. Time and energy spent on mate
3. Breakup optimal gene combinations
iii. Sexual reproduction is the dominate strategy
1. 3 ecological hypotheses for maintenance of sex
1. Unpredictable environmental changes  may
survive (Daphnia)
i. Driving force – abiotic
2. Reduces resource competition within a species
i. Driving force – interspecific interactions
3. Production of rare genotypes  help organisms
escape parasites
i. Driving force – interspecific interactions
ii. Red Queen hypothesis: evolutionary arms
race
1. You need genetic changes to keep
up with adaptations of opponent
2. Sex provides ability to change
UNIT 2
-
Geneti
cs
Lecture About Exam 1:

1) Review exam 1
2) Enhance notes
a. Listen to lecture again
b. Read book
c. Do the questions
3) Go over notes / text
4) Help sessions
a. TA: TWR 1:30-3:30
b. Biology help room M-F 9-12
c. Academic success center
i. Wiley C215
Lecture 9 – Mendelian Genetics
1. Gregor Mendel
a. Blending
b. 1865  genes handed down (no blending)
i. Genes are distinct (no blending)
2. Mendel’s strategy
a. 7 characteristics of peas
i. Flower color, seed shape, things like that
b. Each had 2 contrasting forms
i. Ex two colors, flower and pod position, stem length
ii. One thing or another
 iii.

iv. They are not discontinuous traits

1. One or the other
a. Tall or short
b. Wrinkled or round
c. Purple or white
i. Etc.

c. He would cross parental plants

i. Put pollen from one parent on the stigma of the other with
a paintbrush
d. F1  Seeds  F2 Self fertilization
e. Parental plants  F1 generation  self-fertilize  F2  Seeds
3. Monohybrid cross (p 243)
a. Flower Crossing
i. P – white vs purple flowers
ii. F1 – purple flowers
iii. F2 – 705 purple: 224 white (3:1) ratio
iv. Round Vs wrinkled
1. F1 – round
2. F2 – 5474 round 1850 wrinkled
4. A hypothesis of inheritance – The “law of peas”
1. Alternate forms = alleles
2. Diploid – 2 alleles for each characteristic
3. Pollen/egg/sperm – 1 allele
a. Allele pain segregates during the production of
gametes
4. Alleles different – 1 characteristic is expressed 
dominant allele, 1 masked  recessive allele
5. Genotype vs. Phenotype
a. Location – lows on both homologous chromosomes
b. Multiple forms = alleles
i. Dominant allele R
ii. Recessive allele r
iii. Identical alleles = homozygous RR/rr
iv. Different allele = heterozygous Rr
c. Phenotype – what is expressed (shown in a living thing)
 i. Physical presentation
d. Genotype – genetic makeup (what is in the DNA)
e. P – RR(round) x rr (wrinkled)
f. F1 – Rr (round) x Rr (round)
g. F2 – RR (round), Rr, (round), Rr (round), rr (wrinkled
i. Phenotype 3:1
ii. Genotype 1:2:1

h.
6. Punnett Square
a. Rr x Rr
b. 25% RR, 50% Rr, 25% rr
c. R (sperm) ½ x r (eggs) ½

R r
R RR Rr
R Rr rr

7. Testcross (p 245)
a. Unknown genotype with homozygous recessive
i. R? x rr
b. If RR x rr  Rr dominant phenotype
c. If Rr x rr  1:1 ratio of round vs wrinkled

R r
r Rr rr
r Rr rr

8. Dihybrid Cross
a. P – round yellow seeds x wrinkled green seeds
b. F1 – round 1 yellow seeds
i. Round, yellow (RY) gametes – wrinkled green (ry) gametes
1. 3:1 ratio – linked traits
a. Round, yellow is dominant
ii. Genes separate independently (they are on non-
homologous chromosomes)
1. RY, Ry, rY, ry
a. 9 different genotypes  4 different phenotypes

b. Picture from slide

i. 315 round yellow
ii. 101 wrinkled yellow
iii. 108 round green
iv. 32 wrinkled greed
1. 9:3:3:1 ratio

2.
a. 9 is both dominate traits
b. 1 dominate, 1 recessive
c. 1 recessive, 1 dominate
d. Both recessive
9. Trihybrid Cross (Probability) (p 248)
a. AaBbCc x AaBbCc
i. What’s the probability of a recessive homozygote offspring
(aabbcc)?
1. Deal with the question with -- probability
a. Powerball scenario: 5/69 X 4/68 x 3/67 x 2/66 x
1/65 x 1/26 red = 1 in 292 million
2. Probability = outcome that produces event / total #
of possible outcomes
3. 0  1 Scale (0 to 1)
ii. Rule of multiplication
1. Chance that 2 events occur together is the PRODUCT
of the chances they occur separately
a. EX: getting heads TWICE
i. ½ x ½ = ¼
b. EX: getting 4 girls
 i. ½ x ½ x ½ x ½ = 1/16

iii. Rule of addition

1. Several ways to get the same outcome
a. EX: probability of winning any one combination
i. Getting a 7
1. (1+6) – 1/36
2. (2+5) – 1/36
3. (3+4) – 1/36
4. (4+3) – 1/36
5. (5+2) – 1/36
6. (6+1) – 1/36
a. = 6/36
b. EX: probability of being round
i. RrYy x RrYy
1. PUNNET SQUARE

ii. Prob of RR ¼
 iii. Prob of Rr ½
1. Prob of round = ¾
c. AaBbCc x AaBbCc  aabbcc
d.  8 gametes  8 by 8 Punnett square
i. ABC
ii. ABc
iii. AbC
iv. Abc
v. aBc
vi. ABc
vii. abC
viii. abc
e. Aa x Aa – probability of aa – ½ x ½ = ¼
f. Bb x Bb – probability of bb – ½ x ½ = ¼
g. Cc x Cc – probability of cc – ½ x ½ = ¼
i. aa, bb, cc
ii. ¼ x ¼ x ¼ = 1/64
iii. Multiplication rule
Lecture 10 – Genetics
From Genotype to Phenotype: Some Complications

1. We don’t inherit characters. We inherit Genes

2. Interactions among alleles
1. Incomplete dominance
A) Mendel F1  looked like 1 parent
B) F1 hybrids – intermediate phenotype
C) Red snapdragon x white
 D)
2. Multiple alleles
A) ABO blood type – e alleles / 4 phenotypes

Blood Type Antigen Antibodies

O Neither Anti A / Anti b
A A Anti B
B B Anti A
AB A and B Neither
Both phenotypes in
heterozygote
(codominance) (p
252)
B)

1.
2. O patient: Donor A blood type – No
3. A patient: type O donor (no antigens) – Yes
a. Type O – Universal donor
b. Type AB – Universal recipient

4.
5. O – homozygous recessive
 a. Dominant is not superior
b. Recessive is not superior
3. Interactions among genes
1. Complementation
A) Cross two sweet pea plants (white)  F1: Purple flowers
 F2 9 purple flowers; 7 white
1. 9:3:3:1
2. (both dominant alleles)
B) P: AAbb (white) X aaBB (white)
C) F1: AaBb (purple) X AaBb (purple)
D) F2: 9 purple: 7 white (3+3+1)
1. A—B—
a. Expression dependent on both genes
b. Each gene had veto power

2.
2. Epistasis
A) One gene mask (hides) the effect of the other
B) Only 1 gene has veto power
1. (p253)
C) Gene 1 – Dominant allele (BB/Bb)  black
D) Gene 1 – Homozygous recessive (bb)  chocolate brown
E) Gene 2 – Dominant allele AA/Aa  normal color
F) Gene 2 – blocks all pigment  yellow

1. Aa is epistatic over B gene

a. Aab X AaBb
b. Labs: 9/16 black: 3/16 chocolate labs: 4/16
yellow labs
3. Modifier genes
A) Example – eye color
1. Dominant alle B --? Brown (BB/Bb)
2. Recessive alle bb  blue (bb)
3. Green/grey  blue (bb)
4. Hazel/n\black  brown (BB/Bb)
4. Multiple gene (polygenic of quantitative traits) (p 255)
 A) Example: human height
B) Skin pigmentation (melanin)  3 genes
1. Environmental factors can alter this
a. Sun expose, health, etc.
b. Race is a social construct not a biological one
i. 99.9% identical DNA
5. Pleiotropy (p 252)
A) Single gene – many phenotypic effects
1. Sickle cell anemia
2. White tiger, also cross eyed
3. White cat, usually deaf
4. Interactions between genotype and environment
1. Penetrance and expressivity
A) Penetrance:
1. Genes that are not always expressed
2. Can be variable
3. Percent of individual (usually dominant gene/allele)
carrying a gene  shows expected phenotype
B) Expressivity:
1. Degree to which gene is expressed
a. Usually used by physicians
b. Retinal blastoma – has incomplete penetrance
(dominant allele)
i. Eye tumor
ii. Aa x aa

A a
a Aa aa
a Aa aa
iii. Expect ½ progeny (kids)  have trait
iv. 20% penetrance
1. Don’t expect a 50-50 chance
v. ½ x 20%
1. 10% affinity to show phenotype
2. Himalayan rabbits
a. Raised at room temperature: White, black ears,
black paws, black nose, black tail
b. 5 degrees Celsius  all black
c. 35 degrees Celsius  all white
i. Enzyme thermolabile (does not
work/function at high temps)
 1. Enzyme does not work at these
high temperatures
2. Environment impacts phenotype of
these rabbits
2. Complex traits – multifunctional
A) Mono-zygote twins – identical twins 100% identical DNA
B) Di-zygote twins – fraternal twins 50% identical DNA
(Same as brothers and sisters)
1. If mono-zygote twins share more DNA than di-zygote
twins – then genetics play a role
a. Epigenetics can change things
2. Mono-zygote 100%
3. Di-zygote 50%
4. Siblings 50%
5. Parents/kids 50%
6. Aunts/uncles  niece/ nephew 35%
7. First cousin 12.5

Conclusion: Expression of genes depends on:

1. Overall genetic make-up of

independent (alleles/genes)
2. Environment

Lecture 11 – Patterns of Inheritance

A. HUMAN GENETICS

 Research – e billion base pairs – 21,000 coding genes

 DNA – diagnostics

B. TYPES OF GENETIC DISEASE

 99.9% identical
 Mutation – change in chemical structure of gene
o Ultimate source of genetic variation
1. Single Gene Defects
a. Autosomal (22 human autosomes)
i. Dominate and recessive
b. Sex linked (1 pair of sex chromosomes)
i. Dominant and recessive
2. Chromosomal Disorders
a. Down syndrome
3. Multifactorial Diseases
a. Mental retardation
b. Heart disease
c. Hard to predict

C. HUMAN PEDIGREES

 Family tree
o Circles are females
o Squares are males
o Filled in phenotype of interest
 o Not filled in “normal” phenotype


 Wooly hair – allele W
o Past – ½ normal, ½ wooly hair
o Future –
 Ww X ww
 ½ X ½ X ½ = 1/8 all 3 wooly hair

D. AUTOSOMAL RECESSIVE

 Sickle cell anemia

 Phenylketonuria – (unable to break down phenylalanine)
1. Characteristics
a. Parents are normal
b. Siblings are only affected relatives
c. Males and females are affected at same rate
d. Consanguineous
i. Same blood line / common ancestor / cousins
2. Cystic Fibrosis – Most common autosomal recessive disease
a. 1 in 3000 white newborns in US
b. Mutant protein interferes with cell ability to deal with chloride
c. Thickens secretion
d. Mucus in lungs – blocks airways
i. CF patient without treatment  dies at 5
ii. CF patient with treatment  lives into 40s
e. CF Patient reproduces  1 copy of bad allele
i. 1 in 35 are carriers
ii. Over 1 million people are carriers
1. Cystic Fibrosis Transmembrane Regulator Gene
(CFTR)
2. Patient – 2 copies of abnormal gene
a. No cure
b. Best drug is Trikafta
i. Helps protein fold correctly
ii. $311,000 year
 3. Test carriers – see if you are 2 carriers  ¼ chance
CF child

E. AUTOSOMAL DOMINANT

 Only need 1 bad allele

1. Characteristics
a. Affected individual  ½ normal, ½ affected children
b. Normal children of affected individual  normal children
c. Males and females are affected the same rate
i. Each sex equally likely to transmit gene
2. Huntington's Diseases
a. Disease affects the brain, uncontrollable movements  15-20
years after symptoms

i.
b. 7 per 100,000
c. 30,000 have the disease
d. Incurable disease of nervous system
e. Not expressed until later in life – 30s-40s (late onset)

i.
f. Pre-symptomatic DNA test

1983 – offered a test that would find the “linked marker” on chromosome 4

 Nearby gene that was inherited together

o Restriction enzyme (p 324) – proteins that cut DNA in specific
places
 Venezuela – Lake Maracaibo

1860 – sailor – 7,000 decedents

1990s – found gene – trinucleotide repeat (CAG)n

  9-35 copies – normal
 40-180 copies – HD
o More copies mean the earlier onset it will come
 Outcome of test
o Negative
o Positive
o Reported father is not the biological father
 “Non-paternity event”
 Advantages of test:
o Risk free children
o Ability to plan life – IVF
 Disadvantages of test:
o Loss of hope
o Suicide
o Pressure to take test (insurance companies)

F. SEX-LINKED (X-linked)

 Females – homogenic XX
 Males – heterogenic XY
 X-linked severe combined immunodeficiency syndrome
o Trying gene therapy
 Use retrovirus to add new gene to baby
 Use bone barrow of baby then put it back into baby
 Retrovirus worked but messed up other genes
o Babies later had leukemia
1. Characteristics
i. Ex: Red-green color blindness
b. Higher in males than females
c. Phenotype is never transmitted from father to son
2. Hemophilia – sex-linked recessive (Blood disorder where it can’t clot)
a. 1 in 5000 males
b. Factor 9 not there / doesn’t work
i. Blood can’t clot easily
 ii. (P 321)
c. Queen Victoria – mutation

G. GENETIC SCREENING AND COUNSELING

 Mass predictive screening – for newborns

o 4 million babies get their blood tested
o 34 “care panel” detection
o Genomic sequencing may help us in the future
 Will save parents from emotional pain knowing if their child is going to
struggle or not
 Eugenics  get rid of bad traits
o “Designer babies”

DNA "Fingerprinting"
from Nova Teacher Guide, Fall 1993
The autoradiograph below shows the DNA "fingerprints" of 12 members of a
single family. The two dark bands shown in each column represent two
fragments of each individual's DNA. These fragments will be different lengths
in different people. In this example, each fragment length is designated by a
letter, A through F.

Instructions
Under each individual, write the letter associated with each of the two
markers. This is the individual's genotype. For example, the genotype of the
first son is "C/F". For each child, circle the "letter" inherited from the mother
in red and the "letter" inherited from the father in blue. Then answer the
following questions on a separate sheet.

1. What is one of the "letters" that the missing grandfather must have had?
2. Which "letters" did none of the children inherit from their grandparents?
Why?
3. If the father did not inherit an "F" from his parents, how did an "F" appear
in the next
generation?
4. Suppose that both the father and the paternal grandmother had
retinoblastoma. Which of the children might be at risk for developing
retinoblastoma? Why?
5. Suppose that both the second son and the daughter developed Wilms'
tumor. Which of the other children might also have the DNA sequence with
the gene for this disease? Which parent would they have inherited this
sequence from? Which grandparent would that sequence have come from?
6. How might genetic markers that show differences in the length of DNA
fragments be used to identify
and map genes that predispose someone toward developing cancer?

Lecture 12 – Molecular Basis of Inheritance

A. DEOXYRIBONUCLEIC ACID (p 66-69)

 Alternating sugar and phosphate groups

o Purines (A, G) – 2 fused rings
o Pyrimidines (C, T, U) – 1 ring

B. THE DOUBLE HELIX

1. Chargaff (1947)
a. A=T
b. G=C
i. Complementary
2. Watson-Crick (1953)
a. The double helix
b. 2003  human genome 3 billion base pairs

C. DNA REPLICATION

 A-T / G-C
 1 strand specifies the sequence of new strand
 DNA Helicase – unwinds the strands
o Each old chain acts as template for new chain
1. Meselson and Stahl, 1958
 a. E coli  15N  DNA
i. Break that into 1N
2. Fidelity
a. Add 1,000 nucleotides / second
b. Proofreading enzymes
c. Error rate
d. One in10 billion nucleotides (10^10)
i. E-Coli
1. DNA polymerase –error rate 1 in 10^6 base pairs
2. Mismatch repair / proof reading enzymes
3. Error rate is 1 in every 10^10 bases

D. CENTRAL DOGMA OF MOLECULAR BIOLOGY

 DNA  mRNA  proteins

1. Transcription
a. DNA template recorded
b. RNA polymerase
c. Messenger RNA (mRNA)
i. T—A. U
ii. G—C G
iii. T—A U
iv. A—T A
v. DNA mRNA – leaves nucleus
2. Translation
a. Write from screen here
b. 20 amino acids – 4 nucleotides
c. 4^2 CT AG  16 combinations
d. 3 bases code  codons
3. Genetic code
a. 20 amino acids
b. 3 bases (codon) = amino acid
c. Degenerate
d. Universal genetic language
i. Proline CCC CCU CCA Degenerate
ii. Universal genetic language
4. Translation – The players
a. Ribosomes
b. Messenger RNA (mRNA)
c. Transfer RNA (tRNA)
i. Scaffolding made of r-RNA
 ii. “AUG” – Start codon + RNA
iii. mRNA – CCC (Codon) –
1. (p302)
a. ADD picture
iv. Stop codon UAA, UAG, UGA  peptide released

E. MUTATION

 Rare change in DNA

 Heritable change in genetic material
1. Point Mutations
a. Replace 1 nucleotide with another
i. Silent: has no effect on the protein sequence
1. No change in protein
2. CCC—CCA
ii. Missense
1. Change in amino acids
a. Insignificant
i. Sickle cell anemia disease
ii. Valine in fatal of glamic acid
iii. Nonsense – Stop codon is substituted for an amino acids
2. Frameshift Mutation
a. Addition or deletion of a nucleotide
i. Insertion or deletion of nucleotides may result in a shift in
the reading frame or insertion of a stop codon
1. mRNA read as triplets
3. Causes of Mutation?
a. Spontaneous – error during replication
b. Mutagens – X-rays, smoking
c. Transposable elements – mobile segments of DNA
i. They can insert in the genes and cause problems
 Ultimate and continuous source of new genes
 Rare
 Most mutations have negative consequences
o If DNA was badly copied, then cancer would be in high frequence
o If DNA was perfectly copied  No evolution / no adaptation
 Some mutations are okay and beneficial

 SNPs
o Single nucleotide polymorphisms
 o Inherited variations (point mutations)
o Over 99.9% of our nucleotides are identical, but there are 3
million positions where there is a variation (SNPs)
 Population VS you

C-G C-G
C-G C-G
A-T G-C (SNP here!)
A-T A-T
 Iceland 300,000 people
 De CODE genetics – health geotropic DNA
 Islandiga – app
o Companies (23 and Me) compare you SNPs to people with certain
diseases and assess your probability of getting hundreds of
diseases
o Not very useful yet = biological and clinical
o Finish slide
o “ALL of Use” data here remember
o G.I.N.A.  mew civil rights of century
 Illegal for health in companies

Lecture 13 – Natural Selection

A. Introduction

 1859 Alfred Wallace

 Charles Darwin
 Evolve form ancestorial forms
 Natural Selection
 “Biology does not make sense except in the context of evolution”

B. Lamarck (1809) – adaptations

1. Use and disuse of parts

a. Built-in drive toward perfection
2. Inheritance of acquired characters
a. Modifications are passed to next generation
 i. Giraffe
1. Long necks for food
a. Correct-ish theory
 Correct – earth was old 4.5*109 years
o Gradual adaptation

C. Darwin (and Wallace) – 1858

 “On the origan of Species by Merin of Natural Selection”

 4 observations
a. Exponential growth
b. Pop stable
c. Variation
d. Variation  heritable
a) Not all eggs and sperm  zygotes
a. Not all zygotes  adults
b. Not all adults  reproduce
b) Favorable (better adapted for current environment)

D. Natural Selection

 Process that decides different survival and reproduce of individuals

which have different heritable traits
 N.S. acts on heritable variation expand in phenotype
o Cause  environment (dynamic)
o Inherits individual (genes) not group
o Not for the group of species
1. Consequences
a. Certain phenotypes leave more kids in a particular environment
i. More copies of genes  next generation
ii. Best adapted  more genes to gene pool
iii. Gene pool = total of all genes of all individuals in a
population
iv. Evolution = change in genetic makeup of population
through time
v. All forms of life descended of modifications from
ancestorial species
vi. Natural selection = mechanism

E. Modern theory of Evolution

 o Theory in science  a well-supported body of knowledge that
makes testable predictions
 Ultimate source of variation
o Mutation of DNA (Ultimate source)  new genes / genotypes
(random)
 Population genetics – allele and genotype frequencies changes

F. Industrial Melanin

 Peppered moth – England

 1848 1st black (melanic) moth captured
 1895 – 98% moth melanic or industrial acres
 Trees – light colored lichens
 Bird predation (usually guided predators)
 Industrial reproduction  pollution / salt  trees dark colored
 1950 H.B.D. Kettlewell – mark  release  reproduce
o % reproduced (relative summary of adults)

Light Dark
Unpolluted 12.5% 6.3%
Polluted 1953 13.1% 27.5%
Polluted 1955 25.0% 53.2%
 Current environment
 Liverpool 90% melanic  10% melanic
o Clean air act

G. Microcitoma tuberculosis – bacteria

 Kills 1.6 million / year

 Rifampin – antibiotic used to treat TB
o Targets RNA polymerase – interferes with transcription
 Health problem – being in close proximity with affected individual
o Get bacteria in your lungs  chest pain
o CDC – 13 million – ideal TB (no disease)
 Treatment
 10%  deal with TB disease
 Drug resistant TB (To Rifampin)
o MDR – TB
o EDR – TB
 Drug interferes with transcription
o These have a point mutation in gen rpB – Codes for RNA
polymerase
 Making the drug ineffective
 Changes the configurations of the protein (3D shape) and
prevents binding by the drug Rifampin
 NO  Bacteria developed mutation to deal with drug  NO
o Mutation was predicted in population at low frequency
o Environment with drug  mutant bacteria had advantage
 N.S.  trial by success mechanism
o Wole origin
Lecture 14 – Population Genetics: Hardy-
Weinberg Law

A. GENETICS - ON A LARGE SCALE

 Evolution (Change in the genetic makeup in a population over time)

 Gene pool (genetic makeup of a population)
 Population (group of individuals of the same species in the same area)
o Capable of interbreeding
 o

B. THE GENE POOL

1. Choose your Population

a. 2 populations of fruit flies
i. 60% DD
ii. 40 % dd
b. 60% DD (30 M / 30 F)  D gametes
c. 40% dd (20 M / 20 F)  d gametes
i. 60% gamete  D
ii. 40% gamete  d
2. Results for G2

a.
b. G2 genotype and phototypes differ
i. G1 genotype 60%DD 5-% dd
ii. G2 genotype 36% DD 48% Dd 16% dd
3. Mate G2 Population

a.

C. POPULATION IN GENETIC EQUILIBRIUM

 Allele frequency stayed the same

o .6D .4d
 Affect 1 generation random mating  genotype is stable (genetic
equilibrium)
D. THE HARDY-WEINBERG LAW (p 434-36)

 Single genotype of random mating will produce stable frequencies of

alleles and geotopes under certain conditions.
1. p + q = 1 (100%)
a. (p/q – allele frequencies)
b. P= frequency of dominant alle D
c. Q = frequency of recessive alle d
i. P=.6 and q=.4
2. P^2 + 2pq + q^2 = 1
a. Genotype frequency
b. P^2 = frequency of DD (homozygous dominant)
i. P=.6
ii. P^2=.36
c. Q^2 = frequency of dd (homozygous recessive)
i. Q=.4
ii. Q^2=.26
d. 2pq = frequency of Dd (heterozygous)
i. 2(.6)(.4) = .48
3. An Example - PKU in the U.S.
o 1 in 100,000 babies are born with PKU (Phenylketonuria) 
homozygous recessive
 Autosomal recessive mutation in PAH  Enzyme
 Enzyme that chances phenylalanine to tyrosine
o Patients  restrictive diets which had low phenylalanine
 No protein
o Treatment can help babies to develop normally
o Proportion of carriers in US (heterozygous)
 1/100,000 = .0001 = q^2 (frequency of allele)
 Q = square root of q^2 = 0.01
 2pq = 2(.99) (.01) = 0.0198 about 2%

4. Three Allele - ABO Blood Group

a. Cholera – life-threatening diarrhea – vibrio
i. Severe dehydration
ii. Salt deprecation
 iii. Oral vaccine for it
iv. Kills people where resource poor countries are
b. Type O – susceptible to getting this disease
c. Type A – resistant to cholera (almost immune)
d. 7 great cholera epidemics
i. Why is type O not wiped off the Earth?
e. Malaria
i. Type O – more resistant to parasites
1. More resistant to syphilis
a. Native Americans – high frequency in type O
ii. Genotype and allele frequency with 3 alleles

iii.
iv. P^2 +2pq +2pr + q^2 +2qr +r^2 = 1
1. Genotypes:

a.
2. Phenotypes:

a.
 v.
5. “UNDER CERTAIN CONDITIONS” - 5 ASSUMPTIONS

1. Large Population
2. No Mutation
3. No Migration
a. Genes or people leave a population
4. Random Mating
5. All Genotypes Have Equal Reproductive Success
a. No natural selection
 Baseline to compare actual population
o If allele frequencies change (Hardy-Weinberg assumption doesn’t
hold true)  evolutionary forces are causing the changes
Lecture 15 – Adaptive Evolution: The Role of
Natural Selection

A. INTRODUCTION
  Not in hardy-Weinberg equilibrium – change allele frequency
 Natural selection
o Differential survival and reproduction among phenotypes

B. MODES OF SELECTION (p 437-39)

 Different phenotypes favored

1. Directional Selection
a. One extreme favored

b.
2. Disruptive Selection
a. Both extremes are favored

b.
3. Stabilizing Selection
a. Intermediate is favored
b. Increases average frequency of phenotype
 c.

C. STRENGTH OF SELECTION

 Compare in common environment

 Fitness
o Individuals’ reproduction contribution to next generation
1. Relative Fitness = w̄
a. Survival / reproduction of phenotype compared to phenotype in
particular environment
2. Selection Coefficient = s
a. Selection against inferior genotype
b. 0-1 (1 is lethal)
c. S = 1 - w̄

3.

D. INDUSTRIAL MELANISM

 1848 light moths = 99%

 1895 light moths = 5% 95% dark

1. Polluted Woods

a.
2. Non-Polluted Woods

a.
b. 6.3/13.2 = 0.48
c. .52
d. Strong directional selection
3. Predicted Outcomes
a. Polluted: Allele M approach fixation
i. 100% big M big M
ii. Never going to hit
1. w̄ MM = w̄ Mm
2. Low mutation rate Mm
b. Non-polluted
i. Allele m  approach fixation faster
1. Low mutation rate mM
 ii. Selection acts faster to eliminate “bad” dominant alleles
1. Always exposed to selection
2. Recessive alleles can hide in heterozygous  rarely
eliminated

E. SICKLE CELL ANEMIA

 Autosomal recessive
 100,000 Americans affected
 Change in hemoglobin (O2 carrying around)
 Single base pair change that substitutes A for T
o Change codon in mRNA from gag to gug
o Change Amino Acid  get valine in that spot instead of leunic
acid
 Missense mutation
 Changes the shape and the protein
 Changes red blood shape
 Changes it form disc shape to C-shaped
o Leads to anemia
o Clogs blood vessels
1. The Disease (No malaria)

a.
 b.
2. Malaria – plasmodium (Protista) – transmitted in Red blood cells
a. Anoles mosquitos (p567)
b. Leads to chills/ fever and anemia
c. Over 400,000 people die from malaria
d. HBS allele – resistant to malaria
i. Mutation in rbc change shape and parasite can’t enter

e.
f. Balance between selection pressures
g. Hb5 allele has surprisingly high frequency in Africa due to
malaria
3. Heterozygote Advantage

a.
 i. Environment a – stabilizing selection due to heterozygote
advantage
1. Relative fitness of the heterozygote needs to be 1 (w
= 1)
ii. Environment B – directional selection favoring HB+
1. Hbs decreases slowly because it is hidden in the
heterozygotes
b. Change environments
i. Individual in high malaria (Africa)  move to U.S.
1. Slave trade ran this experiment

ii.
iii. Prevalence of sickle cell allele parallels malaria distribution

F. DOES NATURAL SELECTION LEAD TO PERFECTION?

 Important agent of evolution

o Adapt to current environment
o “Better than”
o Variation does not represent errors
o Compromises – new genes do not arise on demand
Lecture 16: Origins of Genetic Variation

A. Introduction

B. Non-random mating

 Assortative mating: mate similar phenotypes

 Inbreeding: share genes by identical descent


o Excess homozygotes
o Shortage heterozygotes
 o P = # of dominant alleles / total alleles = (37.5*2) +25 / 200 =

0.5 (no change)

 Implications
o Bad recessive alleles come together
o Inbreeding depression – increased frequency of recessive alleles
o Inbreeding – incest taboo
 Chances that sibling have share the same bad alleles is
higher than the person sitting next to you
 First cousin – 12.5% shared DNA
 4-7% of children have birth defects
 3% from parents who are not related
o Assortative mating (Social/religion/ political contrasts)
 Reproductive isolation 
 Sickle cell  native west Africans
 Try-Sachs  E. European Jews
 Albinism  Hopi Indians AZ

C. Mutation – Low Rate / Random

 Point mutation rate 10^-9/pb * 3 * 10^9 (haploid) bp = 3 new point

mutations

D. Migration

 NO immigration (adding genes)

 NO emigration (leaving- lose genes)
o In H-W this was something that had to happen
 Movement of gametes is called: gene flow
o Inc genetic variation  new person comes in and adds genes
 Brown eyed comes into a place with ONLY blue eyes
 GV – Novel genes
o Dec Genetic variation  oppose natural selection
 Make more similar
 GV – homogenize populations

E. Genetic drift

 Change in allele frequency due to chance

o Relative fitness of an allele does not make a difference in
evolutions
 o Important in small populations
 Q = 0.02 for allele X
 Pop = 10^6
o 40,000 copies of X
o (0.02 * 2 * 10^6)
 Pop = 10^2
 4 copies of X
 Pop = 50
 2 copies of X
 Small pq (100 or less)  random figurations of allele frequency
o Concentration biology
 Population bottle neck  founder effect
o When a group colonizes and goes somewhere else
o Ex: old order Amish in Lancaster Pennsylvania was founded by 3
couples in 1770. Since then, there have been a high number of a
rare autosomal disorder called Ellis-van gnarled syndrome
(abnormal skeleton, extra digits, dwarfs, etc.). In 1984, 37% (of
17,000) in this Amish order were carriers for this gene.
 Lower level of genetic variation
 Unusual frequency of rare alleles

F. Evolution: Which Force Did it?

 Testy fly – malathion

o Vector for Protista called Trypanosomes
 Cause African sleeping sickness


o P = .44 ; Q = 0.56  p^2+2pq + q^2 =1
 o M1M1 = 1936 M1M2 = 4928 M2M2 = 3136
o Resistant genotype (M2M2) 1600  3136
o Kill rate reduced  87.6%
 Reduced because you get more resistant flies
 Insect pesticide resistance is an example of
directional selection
o Change in q = .16
o N1= 100,00  N2 = 1000
o Other factors make changes in allele frequencies?
1. Mutation  M2 1*1^-4 *10,00 0= 1 new M2 allele
2. Non-random mating  does not change allele frequency
3. Migration  160 M1M1 leave and 160 M2M2 arrive
a. Very unlikely (usually random exchange with populations)
4. Random error in genetic drift  No (we have a big population)
a. But if population was 50  could recessive alle frequency change
of .16
b. Conclusion – Natural selection but explanation for evolutionary
change

G. Evolutionary Change

1. Factors that increase GV

a. Mutations
i. Introduces variation
b. Sexual reproduction
i. different genetic frequency but no change in allele
frequency
c. Gene flow
i. Ex: Immigration
1. Induce novel alleles
2. Factors that decrease GV
a. Stabilizing selection
i. frequency of average phenotype increases
1. Reduced variation
b. Directional selection
i. Remove allele
1. Fixation of one allele
c. Genetic Drift – often can lose alleles by chance
i. Ex: Small populations
d. Inbreeding
 i. Increase homozygote of genotype but no change of
allele frequency
e. Gene flow
i. homogenize populations

Lecture 17 – Origin of Species

A. DEFINING SPECIES

 Splitting one interbreeding population into two

o Evolution is a branching tree of life

o
1. Biological Species Concept (BSC) (p468)
a. Genetic distinction group of natural populations that share a
gene pool and are reproductively isolated under natural
conditions
b. Actual or potential gene flow – reproductive isolation
2. Limitations
 a. Assumes interbreeding  only asexual reproduction
b. Fossils  can’t mate
c. Breed in lab  not in nature
i. Liger  male lion, female tiger
1. Habitats don’t overlap so it wouldn’t happen in real
life

B. MECHANISMS OF SPECIATION

 Barriers to gene flow

o Split with physical barriers or genetic barriers
1. Allopatric – physical barrier
a. Geographically isolated form parent population
i. Forms new species
1. River, mountain, etc.
b. Splinter group  potential for speciation
c. Favorable conditions for speciation:
i. Population is on the fringe of the species range (different or
more extreme)
ii. Gene pool is different  less GV
iii. Population is small  genetic drift
iv. Different selective pressures (NS)
2. Sympatric (Polyploidy) – genetic barrier
a. Species forms in the midst in the parent population
i. Polyploidy  genome multiplication
1. Many sets of chromosomes
ii. Auto polyploidy  duplication of chromosomes in same
species
1. Non-disjunction
iii. Allopolyploid  combination of chromosomes from 2
different species
1. Hybrid – set of chromosomes from each parent
a. Example:
 b.
c. Common in:
i. Flowering plants
ii. Snails / earthworms
iii. Things that can self-fertilize

C. MAINTAINING SEPARATE GENE POOLS

 2 populations – genetic differentiation

 Reproductive isolating mechanisms (RIMs) (p476-78)
 Prevent gene flow between species
1. Prezygotic – Reduces probability of zygotes mating
a. Habitat isolation
i. Populations live in different habitats
b. Temporal isolations
i. Mating, flowering time, don’t overlap
c. Behavioral isolation
i. Pheromones – attract mates (males)
d. Mechanical isolation
i. Structure differences
e. Gametic isolation
i. Gametes fail to attract
2. Postzygotic – Reduces performance of hybrid that formed
a. Developmental isolation – low zygote variability
b. Hybrid in-viability – adults die before reproduction
c. Hybrid sterility – infertility
i. Mules are sterile and cannot reproduce
ii. Ligers cannot reproduce as well
d. Natural selection favors individuals who do not mismatch species
i. Effective RIMs

D. ADAPTIVE RADIATION
  Emergence of species from common ancestor
 Numerous species from common ancestor introduced to new
environment
1. Darwin’s Finches – Galapagos Islands (p474)
a. Beaks – specialize in different foods
b. 14 species
i. 6 eat seeds
ii. 6 eat insects
iii. 2 eat buds/fruit
c. All evolved from common ancestor – 1 pair of ground finches
i. Storm  islands  founder groups (10,000 years)
ii. Construct new gene pool
1. Allopathic speciation
iii. Reproductive isolation – beak size / shape and different
song characteristics

E. OUTCOMES OF SECONDARY CONTACT

1. Fuse back into one population

2. Continue to diverge
a. Pre-zygote RIMs
3. Hybrid zone
a. Polar bears on land
b. Grizzley bears
i. Grolar bears
1. Happened because of global warming
4. Extinction of one population
5. Hybrid offspring can create a 3rd new species
UNIT 2
-
Geneti
cs
Lecture About Exam 1:

5) Review exam 1
6) Enhance notes
a. Listen to lecture again
b. Read book
c. Do the questions
7) Go over notes / text
8) Help sessions
a. TA: TWR 1:30-3:30
b. Biology help room M-F 9-12
c. Academic success center
i. Wiley C215
Lecture 9 – Mendelian Genetics
10. Gregor Mendel
a. Blending
b. 1865  genes handed down (no blending)
i. Genes are distinct (no blending)
11. Mendel’s strategy
a. 7 characteristics of peas
i. Flower color, seed shape, things like that
b. Each had 2 contrasting forms
i. Ex two colors, flower and pod position, stem length
ii. One thing or another
 iii.

iv. They are not discontinuous traits

1. One or the other
a. Tall or short
b. Wrinkled or round
c. Purple or white
i. Etc.

c. He would cross parental plants

i. Put pollen from one parent on the stigma of the other with
a paintbrush
d. F1  Seeds  F2 Self fertilization
e. Parental plants  F1 generation  self-fertilize  F2  Seeds
12. Monohybrid cross (p 243)
a. Flower Crossing
i. P – white vs purple flowers
ii. F1 – purple flowers
iii. F2 – 705 purple: 224 white (3:1) ratio
iv. Round Vs wrinkled
1. F1 – round
2. F2 – 5474 round 1850 wrinkled
13. A hypothesis of inheritance – The “law of peas”
5. Alternate forms = alleles
6. Diploid – 2 alleles for each characteristic
7. Pollen/egg/sperm – 1 allele
a. Allele pain segregates during the production of
gametes
8. Alleles different – 1 characteristic is expressed 
dominant allele, 1 masked  recessive allele
14. Genotype vs. Phenotype
a. Location – lows on both homologous chromosomes
b. Multiple forms = alleles
i. Dominant allele R
ii. Recessive allele r
iii. Identical alleles = homozygous RR/rr
iv. Different allele = heterozygous Rr
c. Phenotype – what is expressed (shown in a living thing)
 i. Physical presentation
d. Genotype – genetic makeup (what is in the DNA)
e. P – RR(round) x rr (wrinkled)
f. F1 – Rr (round) x Rr (round)
g. F2 – RR (round), Rr, (round), Rr (round), rr (wrinkled
i. Phenotype 3:1
ii. Genotype 1:2:1

h.
15. Punnett Square
a. Rr x Rr
b. 25% RR, 50% Rr, 25% rr
c. R (sperm) ½ x r (eggs) ½

R r
R RR Rr
R Rr rr

16. Testcross (p 245)

a. Unknown genotype with homozygous recessive
i. R? x rr
b. If RR x rr  Rr dominant phenotype
c. If Rr x rr  1:1 ratio of round vs wrinkled

R r
r Rr rr
r Rr rr

17. Dihybrid Cross

a. P – round yellow seeds x wrinkled green seeds
b. F1 – round 1 yellow seeds
i. Round, yellow (RY) gametes – wrinkled green (ry) gametes
1. 3:1 ratio – linked traits
a. Round, yellow is dominant
ii. Genes separate independently (they are on non-
homologous chromosomes)
1. RY, Ry, rY, ry
a. 9 different genotypes  4 different phenotypes

b. Picture from slide

i. 315 round yellow
ii. 101 wrinkled yellow
iii. 108 round green
iv. 32 wrinkled greed
1. 9:3:3:1 ratio

2.
a. 9 is both dominate traits
b. 1 dominate, 1 recessive
c. 1 recessive, 1 dominate
d. Both recessive
18. Trihybrid Cross (Probability) (p 248)
a. AaBbCc x AaBbCc
i. What’s the probability of a recessive homozygote offspring
(aabbcc)?
1. Deal with the question with -- probability
a. Powerball scenario: 5/69 X 4/68 x 3/67 x 2/66 x
1/65 x 1/26 red = 1 in 292 million
2. Probability = outcome that produces event / total #
of possible outcomes
3. 0  1 Scale (0 to 1)
ii. Rule of multiplication
1. Chance that 2 events occur together is the PRODUCT
of the chances they occur separately
a. EX: getting heads TWICE
i. ½ x ½ = ¼
b. EX: getting 4 girls
 i. ½ x ½ x ½ x ½ = 1/16

iii. Rule of addition

1. Several ways to get the same outcome
a. EX: probability of winning any one combination
i. Getting a 7
1. (1+6) – 1/36
2. (2+5) – 1/36
3. (3+4) – 1/36
4. (4+3) – 1/36
5. (5+2) – 1/36
6. (6+1) – 1/36
a. = 6/36
b. EX: probability of being round
i. RrYy x RrYy
1. PUNNET SQUARE

ii. Prob of RR ¼
 iii. Prob of Rr ½
1. Prob of round = ¾
c. AaBbCc x AaBbCc  aabbcc
d.  8 gametes  8 by 8 Punnett square
i. ABC
ii. ABc
iii. AbC
iv. Abc
v. aBc
vi. ABc
vii. abC
viii. abc
e. Aa x Aa – probability of aa – ½ x ½ = ¼
f. Bb x Bb – probability of bb – ½ x ½ = ¼
g. Cc x Cc – probability of cc – ½ x ½ = ¼
i. aa, bb, cc
ii. ¼ x ¼ x ¼ = 1/64
iii. Multiplication rule
Lecture 10 – Genetics
From Genotype to Phenotype: Some Complications

6. We don’t inherit characters. We inherit Genes

7. Interactions among alleles
1. Incomplete dominance
A) Mendel F1  looked like 1 parent
B) F1 hybrids – intermediate phenotype
C) Red snapdragon x white
 D)
2. Multiple alleles
A) ABO blood type – e alleles / 4 phenotypes

Blood Type Antigen Antibodies

O Neither Anti A / Anti b
A A Anti B
B B Anti A
AB A and B Neither
Both phenotypes in
heterozygote
(codominance) (p
252)
B)

1.
2. O patient: Donor A blood type – No
3. A patient: type O donor (no antigens) – Yes
a. Type O – Universal donor
b. Type AB – Universal recipient

4.
5. O – homozygous recessive
 a. Dominant is not superior
b. Recessive is not superior
8. Interactions among genes
1. Complementation
A) Cross two sweet pea plants (white)  F1: Purple flowers
 F2 9 purple flowers; 7 white
1. 9:3:3:1
2. (both dominant alleles)
B) P: AAbb (white) X aaBB (white)
C) F1: AaBb (purple) X AaBb (purple)
D) F2: 9 purple: 7 white (3+3+1)
1. A—B—
a. Expression dependent on both genes
b. Each gene had veto power

2.
2. Epistasis
A) One gene mask (hides) the effect of the other
B) Only 1 gene has veto power
1. (p253)
C) Gene 1 – Dominant allele (BB/Bb)  black
D) Gene 1 – Homozygous recessive (bb)  chocolate brown
E) Gene 2 – Dominant allele AA/Aa  normal color
F) Gene 2 – blocks all pigment  yellow

1. Aa is epistatic over B gene

a. Aab X AaBb
b. Labs: 9/16 black: 3/16 chocolate labs: 4/16
yellow labs
3. Modifier genes
A) Example – eye color
1. Dominant alle B --? Brown (BB/Bb)
2. Recessive alle bb  blue (bb)
3. Green/grey  blue (bb)
4. Hazel/n\black  brown (BB/Bb)
4. Multiple gene (polygenic of quantitative traits) (p 255)
 A) Example: human height
B) Skin pigmentation (melanin)  3 genes
1. Environmental factors can alter this
a. Sun expose, health, etc.
b. Race is a social construct not a biological one
i. 99.9% identical DNA
5. Pleiotropy (p 252)
A) Single gene – many phenotypic effects
1. Sickle cell anemia
2. White tiger, also cross eyed
3. White cat, usually deaf
9. Interactions between genotype and environment
1. Penetrance and expressivity
A) Penetrance:
1. Genes that are not always expressed
2. Can be variable
3. Percent of individual (usually dominant gene/allele)
carrying a gene  shows expected phenotype
B) Expressivity:
1. Degree to which gene is expressed
a. Usually used by physicians
b. Retinal blastoma – has incomplete penetrance
(dominant allele)
i. Eye tumor
ii. Aa x aa

A a
a Aa aa
a Aa aa
iii. Expect ½ progeny (kids)  have trait
iv. 20% penetrance
1. Don’t expect a 50-50 chance
v. ½ x 20%
1. 10% affinity to show phenotype
2. Himalayan rabbits
a. Raised at room temperature: White, black ears,
black paws, black nose, black tail
b. 5 degrees Celsius  all black
c. 35 degrees Celsius  all white
i. Enzyme thermolabile (does not
work/function at high temps)
 1. Enzyme does not work at these
high temperatures
2. Environment impacts phenotype of
these rabbits
2. Complex traits – multifunctional
A) Mono-zygote twins – identical twins 100% identical DNA
B) Di-zygote twins – fraternal twins 50% identical DNA
(Same as brothers and sisters)
1. If mono-zygote twins share more DNA than di-zygote
twins – then genetics play a role
a. Epigenetics can change things
2. Mono-zygote 100%
3. Di-zygote 50%
4. Siblings 50%
5. Parents/kids 50%
6. Aunts/uncles  niece/ nephew 35%
7. First cousin 12.5

Conclusion: Expression of genes depends on:

1. Overall genetic make-up of

independent (alleles/genes)
2. Environment

Lecture 11 – Patterns of Inheritance

A. HUMAN GENETICS

 Research – e billion base pairs – 21,000 coding genes

 DNA – diagnostics

B. TYPES OF GENETIC DISEASE

 99.9% identical
 Mutation – change in chemical structure of gene
o Ultimate source of genetic variation
4. Single Gene Defects
a. Autosomal (22 human autosomes)
i. Dominate and recessive
b. Sex linked (1 pair of sex chromosomes)
i. Dominant and recessive
5. Chromosomal Disorders
a. Down syndrome
6. Multifactorial Diseases
a. Mental retardation
b. Heart disease
c. Hard to predict

C. HUMAN PEDIGREES

 Family tree
o Circles are females
o Squares are males
o Filled in phenotype of interest
 o Not filled in “normal” phenotype


 Wooly hair – allele W
o Past – ½ normal, ½ wooly hair
o Future –
 Ww X ww
 ½ X ½ X ½ = 1/8 all 3 wooly hair

D. AUTOSOMAL RECESSIVE

 Sickle cell anemia

 Phenylketonuria – (unable to break down phenylalanine)
3. Characteristics
a. Parents are normal
b. Siblings are only affected relatives
c. Males and females are affected at same rate
d. Consanguineous
i. Same blood line / common ancestor / cousins
4. Cystic Fibrosis – Most common autosomal recessive disease
a. 1 in 3000 white newborns in US
b. Mutant protein interferes with cell ability to deal with chloride
c. Thickens secretion
d. Mucus in lungs – blocks airways
i. CF patient without treatment  dies at 5
ii. CF patient with treatment  lives into 40s
e. CF Patient reproduces  1 copy of bad allele
i. 1 in 35 are carriers
ii. Over 1 million people are carriers
1. Cystic Fibrosis Transmembrane Regulator Gene
(CFTR)
2. Patient – 2 copies of abnormal gene
a. No cure
b. Best drug is Trikafta
i. Helps protein fold correctly
ii. $311,000 year
 3. Test carriers – see if you are 2 carriers  ¼ chance
CF child

E. AUTOSOMAL DOMINANT

 Only need 1 bad allele

3. Characteristics
a. Affected individual  ½ normal, ½ affected children
b. Normal children of affected individual  normal children
c. Males and females are affected the same rate
i. Each sex equally likely to transmit gene
4. Huntington's Diseases
a. Disease affects the brain, uncontrollable movements  15-20
years after symptoms

i.
b. 7 per 100,000
c. 30,000 have the disease
d. Incurable disease of nervous system
e. Not expressed until later in life – 30s-40s (late onset)

i.
f. Pre-symptomatic DNA test

1983 – offered a test that would find the “linked marker” on chromosome 4

 Nearby gene that was inherited together

o Restriction enzyme (p 324) – proteins that cut DNA in specific
places
 Venezuela – Lake Maracaibo

1860 – sailor – 7,000 decedents

1990s – found gene – trinucleotide repeat (CAG)n

  9-35 copies – normal
 40-180 copies – HD
o More copies mean the earlier onset it will come
 Outcome of test
o Negative
o Positive
o Reported father is not the biological father
 “Non-paternity event”
 Advantages of test:
o Risk free children
o Ability to plan life – IVF
 Disadvantages of test:
o Loss of hope
o Suicide
o Pressure to take test (insurance companies)

F. SEX-LINKED (X-linked)

 Females – homogenic XX
 Males – heterogenic XY
 X-linked severe combined immunodeficiency syndrome
o Trying gene therapy
 Use retrovirus to add new gene to baby
 Use bone barrow of baby then put it back into baby
 Retrovirus worked but messed up other genes
o Babies later had leukemia
3. Characteristics
i. Ex: Red-green color blindness
b. Higher in males than females
c. Phenotype is never transmitted from father to son
4. Hemophilia – sex-linked recessive (Blood disorder where it can’t clot)
a. 1 in 5000 males
b. Factor 9 not there / doesn’t work
i. Blood can’t clot easily
 ii. (P 321)
c. Queen Victoria – mutation

G. GENETIC SCREENING AND COUNSELING

 Mass predictive screening – for newborns

o 4 million babies get their blood tested
o 34 “care panel” detection
o Genomic sequencing may help us in the future
 Will save parents from emotional pain knowing if their child is going to
struggle or not
 Eugenics  get rid of bad traits
o “Designer babies”

DNA "Fingerprinting"
from Nova Teacher Guide, Fall 1993
The autoradiograph below shows the DNA "fingerprints" of 12 members of a
single family. The two dark bands shown in each column represent two
fragments of each individual's DNA. These fragments will be different lengths
in different people. In this example, each fragment length is designated by a
letter, A through F.

Instructions
Under each individual, write the letter associated with each of the two
markers. This is the individual's genotype. For example, the genotype of the
first son is "C/F". For each child, circle the "letter" inherited from the mother
in red and the "letter" inherited from the father in blue. Then answer the
following questions on a separate sheet.

1. What is one of the "letters" that the missing grandfather must have had?
2. Which "letters" did none of the children inherit from their grandparents?
Why?
3. If the father did not inherit an "F" from his parents, how did an "F" appear
in the next
generation?
4. Suppose that both the father and the paternal grandmother had
retinoblastoma. Which of the children might be at risk for developing
retinoblastoma? Why?
5. Suppose that both the second son and the daughter developed Wilms'
tumor. Which of the other children might also have the DNA sequence with
the gene for this disease? Which parent would they have inherited this
sequence from? Which grandparent would that sequence have come from?
6. How might genetic markers that show differences in the length of DNA
fragments be used to identify
and map genes that predispose someone toward developing cancer?

Lecture 12 – Molecular Basis of Inheritance

A. DEOXYRIBONUCLEIC ACID (p 66-69)

 Alternating sugar and phosphate groups

o Purines (A, G) – 2 fused rings
o Pyrimidines (C, T, U) – 1 ring

B. THE DOUBLE HELIX

3. Chargaff (1947)
a. A=T
b. G=C
i. Complementary
4. Watson-Crick (1953)
a. The double helix
b. 2003  human genome 3 billion base pairs

C. DNA REPLICATION

 A-T / G-C
 1 strand specifies the sequence of new strand
 DNA Helicase – unwinds the strands
o Each old chain acts as template for new chain
3. Meselson and Stahl, 1958
 a. E coli  15N  DNA
i. Break that into 1N
4. Fidelity
a. Add 1,000 nucleotides / second
b. Proofreading enzymes
c. Error rate
d. One in10 billion nucleotides (10^10)
i. E-Coli
1. DNA polymerase –error rate 1 in 10^6 base pairs
2. Mismatch repair / proof reading enzymes
3. Error rate is 1 in every 10^10 bases

D. CENTRAL DOGMA OF MOLECULAR BIOLOGY

 DNA  mRNA  proteins

5. Transcription
a. DNA template recorded
b. RNA polymerase
c. Messenger RNA (mRNA)
i. T—A. U
ii. G—C G
iii. T—A U
iv. A—T A
v. DNA mRNA – leaves nucleus
6. Translation
a. Write from screen here
b. 20 amino acids – 4 nucleotides
c. 4^2 CT AG  16 combinations
d. 3 bases code  codons
7. Genetic code
a. 20 amino acids
b. 3 bases (codon) = amino acid
c. Degenerate
d. Universal genetic language
i. Proline CCC CCU CCA Degenerate
ii. Universal genetic language
8. Translation – The players
a. Ribosomes
b. Messenger RNA (mRNA)
c. Transfer RNA (tRNA)
i. Scaffolding made of r-RNA
 ii. “AUG” – Start codon + RNA
iii. mRNA – CCC (Codon) –
1. (p302)
a. ADD picture
iv. Stop codon UAA, UAG, UGA  peptide released

E. MUTATION

 Rare change in DNA

 Heritable change in genetic material
4. Point Mutations
a. Replace 1 nucleotide with another
i. Silent: has no effect on the protein sequence
1. No change in protein
2. CCC—CCA
ii. Missense
1. Change in amino acids
a. Insignificant
i. Sickle cell anemia disease
ii. Valine in fatal of glamic acid
iii. Nonsense – Stop codon is substituted for an amino acids
5. Frameshift Mutation
a. Addition or deletion of a nucleotide
i. Insertion or deletion of nucleotides may result in a shift in
the reading frame or insertion of a stop codon
1. mRNA read as triplets
6. Causes of Mutation?
a. Spontaneous – error during replication
b. Mutagens – X-rays, smoking
c. Transposable elements – mobile segments of DNA
i. They can insert in the genes and cause problems
 Ultimate and continuous source of new genes
 Rare
 Most mutations have negative consequences
o If DNA was badly copied, then cancer would be in high frequence
o If DNA was perfectly copied  No evolution / no adaptation
 Some mutations are okay and beneficial

 SNPs
o Single nucleotide polymorphisms
 o Inherited variations (point mutations)
o Over 99.9% of our nucleotides are identical, but there are 3
million positions where there is a variation (SNPs)
 Population VS you

C-G C-G
C-G C-G
A-T G-C (SNP here!)
A-T A-T
 Iceland 300,000 people
 De CODE genetics – health geotropic DNA
 Islandiga – app
o Companies (23 and Me) compare you SNPs to people with certain
diseases and assess your probability of getting hundreds of
diseases
o Not very useful yet = biological and clinical
o Finish slide
o “ALL of Use” data here remember
o G.I.N.A.  mew civil rights of century
 Illegal for health in companies

Lecture 13 – Natural Selection

A. Introduction

 1859 Alfred Wallace

 Charles Darwin
 Evolve form ancestorial forms
 Natural Selection
 “Biology does not make sense except in the context of evolution”

B. Lamarck (1809) – adaptations

3. Use and disuse of parts

a. Built-in drive toward perfection
4. Inheritance of acquired characters
a. Modifications are passed to next generation
 i. Giraffe
1. Long necks for food
a. Correct-ish theory
 Correct – earth was old 4.5*109 years
o Gradual adaptation

C. Darwin (and Wallace) – 1858

 “On the origan of Species by Merin of Natural Selection”

 4 observations
e. Exponential growth
f. Pop stable
g. Variation
h. Variation  heritable
c) Not all eggs and sperm  zygotes
a. Not all zygotes  adults
b. Not all adults  reproduce
d) Favorable (better adapted for current environment)

D. Natural Selection

 Process that decides different survival and reproduce of individuals

which have different heritable traits
 N.S. acts on heritable variation expand in phenotype
o Cause  environment (dynamic)
o Inherits individual (genes) not group
o Not for the group of species
2. Consequences
a. Certain phenotypes leave more kids in a particular environment
i. More copies of genes  next generation
ii. Best adapted  more genes to gene pool
iii. Gene pool = total of all genes of all individuals in a
population
iv. Evolution = change in genetic makeup of population
through time
v. All forms of life descended of modifications from
ancestorial species
vi. Natural selection = mechanism

E. Modern theory of Evolution

 o Theory in science  a well-supported body of knowledge that
makes testable predictions
 Ultimate source of variation
o Mutation of DNA (Ultimate source)  new genes / genotypes
(random)
 Population genetics – allele and genotype frequencies changes

F. Industrial Melanin

 Peppered moth – England

 1848 1st black (melanic) moth captured
 1895 – 98% moth melanic or industrial acres
 Trees – light colored lichens
 Bird predation (usually guided predators)
 Industrial reproduction  pollution / salt  trees dark colored
 1950 H.B.D. Kettlewell – mark  release  reproduce
o % reproduced (relative summary of adults)

Light Dark
Unpolluted 12.5% 6.3%
Polluted 1953 13.1% 27.5%
Polluted 1955 25.0% 53.2%
 Current environment
 Liverpool 90% melanic  10% melanic
o Clean air act

G. Microcitoma tuberculosis – bacteria

 Kills 1.6 million / year

 Rifampin – antibiotic used to treat TB
o Targets RNA polymerase – interferes with transcription
 Health problem – being in close proximity with affected individual
o Get bacteria in your lungs  chest pain
o CDC – 13 million – ideal TB (no disease)
 Treatment
 10%  deal with TB disease
 Drug resistant TB (To Rifampin)
o MDR – TB
o EDR – TB
 Drug interferes with transcription
o These have a point mutation in gen rpB – Codes for RNA
polymerase
 Making the drug ineffective
 Changes the configurations of the protein (3D shape) and
prevents binding by the drug Rifampin
 NO  Bacteria developed mutation to deal with drug  NO
o Mutation was predicted in population at low frequency
o Environment with drug  mutant bacteria had advantage
 N.S.  trial by success mechanism
o Wole origin
Lecture 14 – Population Genetics: Hardy-
Weinberg Law

A. GENETICS - ON A LARGE SCALE

 Evolution (Change in the genetic makeup in a population over time)

 Gene pool (genetic makeup of a population)
 Population (group of individuals of the same species in the same area)
o Capable of interbreeding
 o

B. THE GENE POOL

4. Choose your Population

a. 2 populations of fruit flies
i. 60% DD
ii. 40 % dd
b. 60% DD (30 M / 30 F)  D gametes
c. 40% dd (20 M / 20 F)  d gametes
i. 60% gamete  D
ii. 40% gamete  d
5. Results for G2

a.
b. G2 genotype and phototypes differ
i. G1 genotype 60%DD 5-% dd
ii. G2 genotype 36% DD 48% Dd 16% dd
6. Mate G2 Population

a.

C. POPULATION IN GENETIC EQUILIBRIUM

 Allele frequency stayed the same

o .6D .4d
 Affect 1 generation random mating  genotype is stable (genetic
equilibrium)
D. THE HARDY-WEINBERG LAW (p 434-36)

 Single genotype of random mating will produce stable frequencies of

alleles and geotopes under certain conditions.
5. p + q = 1 (100%)
a. (p/q – allele frequencies)
b. P= frequency of dominant alle D
c. Q = frequency of recessive alle d
i. P=.6 and q=.4
6. P^2 + 2pq + q^2 = 1
a. Genotype frequency
b. P^2 = frequency of DD (homozygous dominant)
i. P=.6
ii. P^2=.36
c. Q^2 = frequency of dd (homozygous recessive)
i. Q=.4
ii. Q^2=.26
d. 2pq = frequency of Dd (heterozygous)
i. 2(.6)(.4) = .48
7. An Example - PKU in the U.S.
o 1 in 100,000 babies are born with PKU (Phenylketonuria) 
homozygous recessive
 Autosomal recessive mutation in PAH  Enzyme
 Enzyme that chances phenylalanine to tyrosine
o Patients  restrictive diets which had low phenylalanine
 No protein
o Treatment can help babies to develop normally
o Proportion of carriers in US (heterozygous)
 1/100,000 = .0001 = q^2 (frequency of allele)
 Q = square root of q^2 = 0.01
 2pq = 2(.99) (.01) = 0.0198 about 2%

8. Three Allele - ABO Blood Group

a. Cholera – life-threatening diarrhea – vibrio
i. Severe dehydration
ii. Salt deprecation
 iii. Oral vaccine for it
iv. Kills people where resource poor countries are
b. Type O – susceptible to getting this disease
c. Type A – resistant to cholera (almost immune)
d. 7 great cholera epidemics
i. Why is type O not wiped off the Earth?
e. Malaria
i. Type O – more resistant to parasites
1. More resistant to syphilis
a. Native Americans – high frequency in type O
ii. Genotype and allele frequency with 3 alleles

iii.
iv. P^2 +2pq +2pr + q^2 +2qr +r^2 = 1
1. Genotypes:

a.
2. Phenotypes:

a.
 v.
10. “UNDER CERTAIN CONDITIONS” - 5 ASSUMPTIONS

6. Large Population
7. No Mutation
8. No Migration
a. Genes or people leave a population
9. Random Mating
10. All Genotypes Have Equal Reproductive Success
a. No natural selection
 Baseline to compare actual population
o If allele frequencies change (Hardy-Weinberg assumption doesn’t
hold true)  evolutionary forces are causing the changes
Lecture 15 – Adaptive Evolution: The Role of
Natural Selection

A. INTRODUCTION
  Not in hardy-Weinberg equilibrium – change allele frequency
 Natural selection
o Differential survival and reproduction among phenotypes

B. MODES OF SELECTION (p 437-39)

 Different phenotypes favored

4. Directional Selection
a. One extreme favored

b.
5. Disruptive Selection
a. Both extremes are favored

b.
6. Stabilizing Selection
a. Intermediate is favored
b. Increases average frequency of phenotype
 c.

C. STRENGTH OF SELECTION

 Compare in common environment

 Fitness
o Individuals’ reproduction contribution to next generation
4. Relative Fitness = w̄
a. Survival / reproduction of phenotype compared to phenotype in
particular environment
5. Selection Coefficient = s
a. Selection against inferior genotype
b. 0-1 (1 is lethal)
c. S = 1 - w̄

6.

D. INDUSTRIAL MELANISM

 1848 light moths = 99%

 1895 light moths = 5% 95% dark

4. Polluted Woods

a.
5. Non-Polluted Woods

a.
b. 6.3/13.2 = 0.48
c. .52
d. Strong directional selection
6. Predicted Outcomes
a. Polluted: Allele M approach fixation
i. 100% big M big M
ii. Never going to hit
1. w̄ MM = w̄ Mm
2. Low mutation rate Mm
b. Non-polluted
i. Allele m  approach fixation faster
1. Low mutation rate mM
 ii. Selection acts faster to eliminate “bad” dominant alleles
1. Always exposed to selection
2. Recessive alleles can hide in heterozygous  rarely
eliminated

E. SICKLE CELL ANEMIA

 Autosomal recessive
 100,000 Americans affected
 Change in hemoglobin (O2 carrying around)
 Single base pair change that substitutes A for T
o Change codon in mRNA from gag to gug
o Change Amino Acid  get valine in that spot instead of leunic
acid
 Missense mutation
 Changes the shape and the protein
 Changes red blood shape
 Changes it form disc shape to C-shaped
o Leads to anemia
o Clogs blood vessels
4. The Disease (No malaria)

a.
 b.
5. Malaria – plasmodium (Protista) – transmitted in Red blood cells
a. Anoles mosquitos (p567)
b. Leads to chills/ fever and anemia
c. Over 400,000 people die from malaria
d. HBS allele – resistant to malaria
i. Mutation in rbc change shape and parasite can’t enter

e.
f. Balance between selection pressures
g. Hb5 allele has surprisingly high frequency in Africa due to
malaria
6. Heterozygote Advantage

a.
 i. Environment a – stabilizing selection due to heterozygote
advantage
1. Relative fitness of the heterozygote needs to be 1 (w
= 1)
ii. Environment B – directional selection favoring HB+
1. Hbs decreases slowly because it is hidden in the
heterozygotes
b. Change environments
i. Individual in high malaria (Africa)  move to U.S.
1. Slave trade ran this experiment

ii.
iii. Prevalence of sickle cell allele parallels malaria distribution

F. DOES NATURAL SELECTION LEAD TO PERFECTION?

 Important agent of evolution

o Adapt to current environment
o “Better than”
o Variation does not represent errors
o Compromises – new genes do not arise on demand
Lecture 16: Origins of Genetic Variation

A. Introduction

B. Non-random mating

 Assortative mating: mate similar phenotypes

 Inbreeding: share genes by identical descent


o Excess homozygotes
o Shortage heterozygotes
 o P = # of dominant alleles / total alleles = (37.5*2) +25 / 200 =

0.5 (no change)

 Implications
o Bad recessive alleles come together
o Inbreeding depression – increased frequency of recessive alleles
o Inbreeding – incest taboo
 Chances that sibling have share the same bad alleles is
higher than the person sitting next to you
 First cousin – 12.5% shared DNA
 4-7% of children have birth defects
 3% from parents who are not related
o Assortative mating (Social/religion/ political contrasts)
 Reproductive isolation 
 Sickle cell  native west Africans
 Try-Sachs  E. European Jews
 Albinism  Hopi Indians AZ

C. Mutation – Low Rate / Random

 Point mutation rate 10^-9/pb * 3 * 10^9 (haploid) bp = 3 new point

mutations

D. Migration

 NO immigration (adding genes)

 NO emigration (leaving- lose genes)
o In H-W this was something that had to happen
 Movement of gametes is called: gene flow
o Inc genetic variation  new person comes in and adds genes
 Brown eyed comes into a place with ONLY blue eyes
 GV – Novel genes
o Dec Genetic variation  oppose natural selection
 Make more similar
 GV – homogenize populations

E. Genetic drift

 Change in allele frequency due to chance

o Relative fitness of an allele does not make a difference in
evolutions
 o Important in small populations
 Q = 0.02 for allele X
 Pop = 10^6
o 40,000 copies of X
o (0.02 * 2 * 10^6)
 Pop = 10^2
 4 copies of X
 Pop = 50
 2 copies of X
 Small pq (100 or less)  random figurations of allele frequency
o Concentration biology
 Population bottle neck  founder effect
o When a group colonizes and goes somewhere else
o Ex: old order Amish in Lancaster Pennsylvania was founded by 3
couples in 1770. Since then, there have been a high number of a
rare autosomal disorder called Ellis-van gnarled syndrome
(abnormal skeleton, extra digits, dwarfs, etc.). In 1984, 37% (of
17,000) in this Amish order were carriers for this gene.
 Lower level of genetic variation
 Unusual frequency of rare alleles

F. Evolution: Which Force Did it?

 Testy fly – malathion

o Vector for Protista called Trypanosomes
 Cause African sleeping sickness


o P = .44 ; Q = 0.56  p^2+2pq + q^2 =1
 o M1M1 = 1936 M1M2 = 4928 M2M2 = 3136
o Resistant genotype (M2M2) 1600  3136
o Kill rate reduced  87.6%
 Reduced because you get more resistant flies
 Insect pesticide resistance is an example of
directional selection
o Change in q = .16
o N1= 100,00  N2 = 1000
o Other factors make changes in allele frequencies?
5. Mutation  M2 1*1^-4 *10,00 0= 1 new M2 allele
6. Non-random mating  does not change allele frequency
7. Migration  160 M1M1 leave and 160 M2M2 arrive
a. Very unlikely (usually random exchange with populations)
8. Random error in genetic drift  No (we have a big population)
a. But if population was 50  could recessive alle frequency change
of .16
b. Conclusion – Natural selection but explanation for evolutionary
change

G. Evolutionary Change

3. Factors that increase GV

a. Mutations
i. Introduces variation
b. Sexual reproduction
i. different genetic frequency but no change in allele
frequency
c. Gene flow
i. Ex: Immigration
1. Induce novel alleles
4. Factors that decrease GV
a. Stabilizing selection
i. frequency of average phenotype increases
1. Reduced variation
b. Directional selection
i. Remove allele
1. Fixation of one allele
c. Genetic Drift – often can lose alleles by chance
i. Ex: Small populations
d. Inbreeding
 i. Increase homozygote of genotype but no change of
allele frequency
e. Gene flow
i. homogenize populations

Lecture 17 – Origin of Species

A. DEFINING SPECIES

 Splitting one interbreeding population into two

o Evolution is a branching tree of life

o
3. Biological Species Concept (BSC) (p468)
a. Genetic distinction group of natural populations that share a
gene pool and are reproductively isolated under natural
conditions
b. Actual or potential gene flow – reproductive isolation
4. Limitations
 a. Assumes interbreeding  only asexual reproduction
b. Fossils  can’t mate
c. Breed in lab  not in nature
i. Liger  male lion, female tiger
1. Habitats don’t overlap so it wouldn’t happen in real
life

B. MECHANISMS OF SPECIATION

 Barriers to gene flow

o Split with physical barriers or genetic barriers
3. Allopatric – physical barrier
a. Geographically isolated form parent population
i. Forms new species
1. River, mountain, etc.
b. Splinter group  potential for speciation
c. Favorable conditions for speciation:
i. Population is on the fringe of the species range (different or
more extreme)
ii. Gene pool is different  less GV
iii. Population is small  genetic drift
iv. Different selective pressures (NS)
4. Sympatric (Polyploidy) – genetic barrier
a. Species forms in the midst in the parent population
i. Polyploidy  genome multiplication
1. Many sets of chromosomes
ii. Auto polyploidy  duplication of chromosomes in same
species
1. Non-disjunction
iii. Allopolyploid  combination of chromosomes from 2
different species
1. Hybrid – set of chromosomes from each parent
a. Example:
 b.
c. Common in:
i. Flowering plants
ii. Snails / earthworms
iii. Things that can self-fertilize

C. MAINTAINING SEPARATE GENE POOLS

 2 populations – genetic differentiation

 Reproductive isolating mechanisms (RIMs) (p476-78)
 Prevent gene flow between species
3. Prezygotic – Reduces probability of zygotes mating
a. Habitat isolation
i. Populations live in different habitats
b. Temporal isolations
i. Mating, flowering time, don’t overlap
c. Behavioral isolation
i. Pheromones – attract mates (males)
d. Mechanical isolation
i. Structure differences
e. Gametic isolation
i. Gametes fail to attract
4. Postzygotic – Reduces performance of hybrid that formed
a. Developmental isolation – low zygote variability
b. Hybrid in-viability – adults die before reproduction
c. Hybrid sterility – infertility
i. Mules are sterile and cannot reproduce
ii. Ligers cannot reproduce as well
d. Natural selection favors individuals who do not mismatch species
i. Effective RIMs

D. ADAPTIVE RADIATION
  Emergence of species from common ancestor
 Numerous species from common ancestor introduced to new
environment
2. Darwin’s Finches – Galapagos Islands (p474)
a. Beaks – specialize in different foods
b. 14 species
i. 6 eat seeds
ii. 6 eat insects
iii. 2 eat buds/fruit
c. All evolved from common ancestor – 1 pair of ground finches
i. Storm  islands  founder groups (10,000 years)
ii. Construct new gene pool
1. Allopathic speciation
iii. Reproductive isolation – beak size / shape and different
song characteristics

E. OUTCOMES OF SECONDARY CONTACT

6. Fuse back into one population

7. Continue to diverge
a. Pre-zygote RIMs
8. Hybrid zone
a. Polar bears on land
b. Grizzley bears
i. Grolar bears
1. Happened because of global warming
9. Extinction of one population
10. Hybrid offspring can create a 3rd new species
UNIT
3
Lecture 19 - Patterns of Population Growth

A. WHY STUDY POPULATION GROWTH?

1. Population = interbreeding organisms of SAME species in same
area
2. Why?
3. Predict growth trends
4. Indicator of ecological conditions
 5. Interactions / biotic / abiotic environment
B. EXPONENTIAL GROWTH
 Uncontrolled growth
 Rate depends on the # of individuals
 Can’t maintain exponential grown (resource limitations)
 Resources are abundant – invasion by opportunistic species
(species that come into a new environment like a weed or insect)

1. Discrete
i. Discrete units of time
1. When first son was about 5, they wanted help, he
wanted money. They have him set the table for a
penny. Next day he sets it and asks for 2 pennies.
What if he doubles his fee every day?
a. Day 0 – 1 cent
b. Day 1 – 2 cents
c. Day 3 – 4 cents
d. Day 4 – 8 cents
i. Equation: N=N0R0^T
1. R0 = net reproductive rate (#
female produced / current female)
2. N = population size (future)
3. N0 = initial population size
4. T = time
ii. N = (0.01) * 2^30 = $10,737,418.20
(Day 30)
e. Breed once – non-overlapping breeders
f. Moth: R0=1.9 N0=600 T=2 years
i. N=600 * (1.9)^2=2166
2. Continuous – overlapping generations / breed repeatedly
i. Change of N / Change of T = rN
ii. Change of N/ Change of T = # of individuals / rate of time
iii. N = # of individuals in population
iv. R = intrinsic rate of increase = birth – death
1. Head lice:
a. R = .028 / day
b. N = 1000 adults
c. =.028 * (1000) = 28 / day
d. N=N0e^rT
i. N=1000e^9.028)(5)
 1. 1150 head lice on day 5
3. Recap of Equations

i.
C. Net Reproductive rate vs intrinsic rate of increase - R0 vs r

Population size R0 = # of female r=b-d

produced / current
females
Decreasing Less than 1 Less than 0
(negative)
Constant 1 0
Increasing More than 1 More than 0
(postive)

D. LOGISTIC GROWTH (p 1175)

 Restricted growth
o Carrying capacity of the environment (K)

o
 o
o R = feature of species
o K = feature of environment
 K can change during population overshoot of K
 Cattle 1880’s – overgrazed K decreased
 Reindeer on St. Paul island
 4 males, 22 females in 1910


1. Carrying Capacity
2. Maximum Growth Rate
E. POPULATION REGULATION
1. Density Independent
i. Not influenced by population size
2. Density Dependent
i. Depends on population size
1. Effect increases as population size increases (biotic)
ii. Zebra mussels – new species introduced to the great lakes
1. They had no predators or no competitors
a. Exponentially increased population size over 25
years
Lecture 20 - Demography and Life History
Strategies

A. INTRODUCTION
 Demography – vital statistics that affect population size and
growth
 Nfuture = N0 + B – D + I - E
B. SURVIVORSHIP – age specific
 Image of mortality
 Ix – population of cohort surviving to age “x”

 I1 = 0.1
 I2 (0.1)(0.1)
 I3 (0.1)(0.1) (0.1)
1. Survivorship Curves
i. Survivorship can vary
1. Among species – Dogs live 8-15 years
2. Between sexes – female survival > male survival

a.
3. Different environmental conditions (developed /
developed nations)
a. Hygiene, diet, medicines
i. Life span: U.S. #48 in the world
ii. Survivorship curve (p 1177)
1. Plot log10 of survivorship against time
a. Semi-log paper
i. Log linear plot
a) Type 1 – low mortality until old age, few young
a. Ex: humans in developed countries
b. K-selected
b) Type 2 – constant mortality trough life
a. Ex: lizards, birds
c) Type 3 – very high juvenal mortality, many offspring
a. Ex: fish, plants, insects
b. R-selected
C. FECUNDITY
1. Age specific fecundity
2. Mx = # of daughters / females at age x
i. Consider only females
D. LIFE TABLE
1. Inspect population demographic parameters
2. R0= net reproductive rate = l1m1 + l2m2

3.
4. R0 = average # of females produced by females in a lifetime
E. AGE DISTRIBUTIONS
1. Graphical representatives of proportion of population at each age
class

2.

3.
F. LIFE HISTORY STRATEGIES
 Life history – characteristics affect survival / reproduction
 Not necessarily highest r – trade-offs
 Can you reproduce forever?
o No
o Negative correlation between current fecundity and
probably of future survival
 Derange expect to see if birds adjust to catch size to maximize
reproductive success


 Life history traits form a continuum
1. r-Selected Strategy
i. Opportunistic – geared towards rapid completion of life
cycle in unpredictable environments
ii. High r value – reproduce early and often
iii. Density independent
2. K-Selected Strategy
i. Opportunistic – equilibrium
ii. Compete for resources in a stable environment (k)
iii. Few, well provisioned offspring
iv. Density dependent
3. Comparison

4.

5.
Lecture 21 – Human Population Growth

A. Introduction

B. Over 8 Billion Served

 About 10,000 years ago we had a growth surge due to agriculture

 BC/AD 250 million
 1650 500 million
o Scientific/ industrial advancement
o 1804 1 billion
o 1930 2 billion
 125 years to add billion
o 1960 3 billion
o 1975 4 billion
 o 1987 5 billion
o 1999 6 billion
o 2011 7 billion
o 2022 8 billion
 Population of earth has doubled over the past 50 years
1. Rate of increase
i. About every minute 260 babies are born
ii. 120 die
iii. 140 people added
1. B=20/1000=0.020
2. D=8/1000=0.008
a. R=b-d=0.012
i. 1.2% growth

b.
2. Doubling Time

a.

b.

C. Growth Patterns

 70’s  r=0.020 , dt about 35 years for the world

1. World population growing r>0
2. Developed nations are reducing r (Italy/Spain/Japan)
3. Developing nations r is still high  98% of growth of population 
developing nation
4. Asia has a lot of people
a. China – 1.4 billion
b. India – 1.4 billion
 India
 Egypt
 Congo
  Pakistan
 Nigeria
 Ethiopia
 Philippians
 Tanzania

D. Causes of Population Growth

1. Demographic Transitions
a. Relationship between population growth and development of a
country
b. Death rate goes down  sanitary/medical/nutrition
c. Birth rate remains high

d. Why does b drop as far as d

i. Historical
ii. Children – labor farms
iii. Desire to increase group
iv. Children (sons) = prestige
v. Lack of knowledge
1. Birth control, government control, etc
e. Women education is crucial to sustainable development
i. Increase in female literacy
1. decrease mortality rate of children under 5
a. Educated women make better choices
2. Fertility rate goes down
3. Empower women  with education
f. Population growth  developing nations (poorest)
i. American will do 20-100 times more environmental
damage
2. Age Structure
a. Each couple only had 2 children  population growth would stop
i. Not right away
b. Sweden is stable, Mexico is growing
 i. Even if you set r=0 tomorrow in India – mandating of
population growth would continue to increase for 30 years
(future reproducers)
1. Bottom has a lot of kids that will reproduce

ii.

E. Human Population Growth Will Stop

a) Food production in East Africa

1. Increase death rate?
a. 12% of population  chronically undernourished
b. ½ of people that die in Africa are under 5 years old
i. Nutrition, sickness, etc
ii. 37 megacities (Over 10 million people)
1. UN predicts more growth in African cities
a. Urban areas increase
2. Seven challenges
1. Agriculture productivity
2. Non-renewable resources (Fossil Fuels)
a. CO2 levels are increasing rapidly
3. Loss of biodiversity
a. Habitat destruction = species dying = extinction
4. Pollutants
a. Affect our health, stuff like lead and pesticides
b. 9 million premature deaths due to pollutants
5. Water Stress
a. Gets worse and worse
6. Desertification
a. Lose topsoil and become a desert
b. Becomes inhabitable
7. Climate change
a. Created by CO2 emissions
b. Greatest impact is the people who are the least
responsible for it
 Estimated K (carrying capacity) for earth
  K= few billion people

Lecture 22 – Interactions Among Populations

A. THE POSSIBILITIES

 Ecological interactions  species act together

 Competition
 Predation
 Parasitism
 Mutualism
 Commensalism
 Amensalism
 

 Species interactions are often dynamic (changing) and asymmetrical

and sometimes they result in evolutionary change

B. THE ECOLOGICAL NICHE

 Range of biotic / abiotic conditions within which an organism can

survive and reproduce
 Fundamental niche
o All the resources an organism can you (theoretically) when no
other organisms are around
 o Realized Niche – portion of fundamental niche utilized

1. Competitive Exclusion Principle

a. Gause
b. Limit to niche overlap that allows two species to exist

C. COMPETITION

 Use same resources

o Short supply – limited
 Mutually negative
o Both species do worse
 Interspecific – among species
 Intraspecific – within species
a. Exploitation – obtain and use up resources
a. Grahm eats the pizza before anyone else gets it
b. Plants use poising (toxin) to kill plants
i. Spotted knapweed
b. Interference – actively prevent competition from resources

D. OUTCOMES OF COMPETITION

 Competitive exclusion – one species becomes locally extinct

o European staling’s – Introduced to NYC in 1891 and compete with
blue birds. They beat the blue birds and human intervention was
needed
 Either specifies wins depending on environmental conditions
o Competitive abilities of two participants are relative
 Depends on environment
  Stable coexist of both species
o Resource portioning
o Character displacement

E. COMPETITION IN THE LABORATORY

1. Paramecium – Gause (Outcome #1)

a. He has two species: P. aurelia and P. Caudatum.
b. They were grown alone and then mixed
i. Alone  grow in a logistic matter (until carrying compacity)
ii. Grow together  compete too much and are both harmed

iii.
2. Flour Beetles – Park (Outcome #2)
a. T. castaniam: did better in hot/moist conditions
b. T. Confusum: did better in cool/dry conditions

F. COMPETITION IN NATURE

1. Resource partitioning (Outcome #3)

a. Warblers – MacArthur
i. 5 warbler species (sympatric: in the same place)
ii. Feeding habits differed
1. They eat insects in different parts
a. Niche differentiation  guild  group that uses
the same resources in different ways
 b.

2. Character displacement
a. Change in species traits depending on weather they are
competing for resources
i. Allopatric / sympatric with competitor
b. Sphagnum Moss

c.
3. Barnacles – Connell
a. Chthamulus – upper
b. Semi Balanus – lower
i. Removes semi balaunus – chthamuls settle everywhere
ii. removes chthamulus – no change in distribution
c. Balanus cannot live in low tide area
i. Crowds out chthamulus – outcompete
 d.

G. MUTUALISM (+,+)

 Both species benefit

 Endosymbiotic hypothesis – Lynn Marguto (1970)
o Prokaryote took up resistance in others
 Chloroplasts/mitochondria  eukaryotic cells
1. Nitrogen-Fixing Bacteria
a. 79% of the air is nitrogen
i. Nitrogen has a triple covalent bond which is hard to break
ii. N2 +8H2  2NH3 +H2
iii. Rhizobium – invade roots of legumes
1. Fix nitrogen from air / release excess
b. Mutualism:
i. Rhizobium – supplies nitrogen
ii. Plants – supply sugar from PHS / nodules (anerobic)
2. Ants and Acacia Trees
a. Interaction happens in Central America
i. Janzen  data

ii.
iii. Acacia has large hollow thorns  nests for ants
iv. Nectar at base of leaves
v. Ants are active 24/7 and acacia trees have the nectar year
round
1. Both have maximized the benefit of mutualism
a. Coevolution
Homework 4 Ethics Question:

Some people regard the rapid population growth of developing countries as our
most serious environmental problem. Others think that the population growth in
industrialized countries, though smaller, is actually a greater threat to the
environment. What kinds of problems result from population growth in:

A. Developing countries?

 Deforestation: More land is destroyed to create housing and agriculture sites

which leads to loss of biodiversity
 Running out of resources: The increase in demand for food, water, and energy
will deplete resources faster
 Pollution: More people in growing populations can lead to pollution in water
and air
 Health issues: Overcrowding of people can lead to poor health and make
diseases able to spread faster

B. The industrialized world?

 Higher carbon emissions: More people in industrialized areas means that

more people will be contributing to more greenhouse gas emissions
 Excessive Waste: Industrialized areas already have problems with effectively
getting rid of waste and trash and adding more people would only speed up
the problem
 Habitat Loss: Development of houses and other constructions reduce natural
habitats and affect the biodiversity of the land
 Excessive Water Usage: The need for water will dramatically increase and it
becomes easier for bodies of water to become polluted quicker

C. Which do you think is the greater threat and why? Use the 7-step strategy to
explain your reasoning.

1. State the Problem:

a. The problem is determining if population growth in developing
countries or industrialized countries is a more significant
environmental threat.
2. Check the Facts:
a. Developing countries have high population growth rate which can lead
to pollution, deforestation, and resource scarcity.
b. Industrialized countries have a slower population growth but consume
more resources and have higher carbon footprints.
3. Identify Affected Parties:
a. People – in developing and industrialized countries due to rapid growth
and increasing pollution
 b. Earth – Increase in human population has led to lack of biodiversity,
habitat loss, pollution in the air and water, trash that is unable to be
destroyed, etc.
4. Develop List of Options:
a. Focus on efforts and incentives to limit population growth
i. Ex: 1 child policy
b. Implement stricter resource consumption laws
i. Ex: Limit the water, gas, etc a person/family can use
c. Limit emission controls
i. Ex: (In industrialized areas) limit gas cars and push for electric
cars
ii. Ex: Limit the amount of non-renewable resources people use
d. Promote sustainable growth
i. Ex: Making sure everyone has what they need to survive and
have a steady growth rate that is able to be planned and
prepared for
5. Test Options:
a. Harm Test: Option 1 does more harm because it prevents families from
feeling safe and like they have the option to grow their family the way
they want
b. Publicity Test: If I chose to limit emission controls, I would want this to
be published because it would most likely be received well
6. Construct Desired Option(s):
a. Limit emission controls
i. Promote carbon reduction in industrialized countries
ii. Encourage developing nations to adopt sustainable energy
practices
iii. Invest in renewable energy around the world
1. A downfall could be the level of commitment person to
person and country to country
7. Take Action:
a. I would implement “Limiting Emissions” since I feel like it is something
that everyone can do no matter what. This would help both
industrialized and developing nations to help clean up their pollution
and promote better use of energy.

Overall, I feel that rapid population growth in industrialized nations is far worse than
rapid population growth in developing countries. This is because in industrialized
nations contribute to a much higher carbon footprint and pollution rate. Therefore if
population was to rapidly grow there, it would be more harmful than if a population
in a developing nation grew.
Lecture 23 – Coevolution

A. Predation

1. Arms Race
a. Leads to mutual selective pressures (Red Queen)
2. Prey avoidance adaptations (pg 1190-92)
a. Poison
i. Monarch butterflies
ii. Plants – defense against herbivores
 b. Apocentric coloration – wearying coloration
c. Mimicry (Bateson)
i. Mimicry of dangerous species by ones that are not
1. King snake – fine
2. Coral snake = venomous
a. Both look VERY similar
d. Mullenam mimicry
i. Both species distasteful (mutualism)
e. Cryptic coloration
i. Peppered moths
f. Escape in time/space
i. Unpredictable
g. Escape in size
i. Rhinos
h. Early detection
i. Moths (hunted by bats and can hear well and dive quickly)
i. Inducible defense
i. Muscles – when crabs are around, they look like they have
bigger / thicker shells
B. Outcomes of Predation
 Cyclic changes in population size
a. Predator population size fluctuates less than prey population size
b. Cycles are out of phase
1. Hare/lynx Oscillations (pg 1195)
a. 10-year oscillation cycle
i. Predation drives cycles

ii.
2. Protozoa – Gause
a. Paramecium caudation – prey
b. Didimen naturium – predator
 c. Simple system: 4-5 drops to extinction
d. Sediment – refuge for prey  no stable cycles
3. Mites – Huffaker
a. 2 species of mites – predator / prey (orange)
i. 40 orange universes
1. Predator overate the prey and drove them to
extinction
2. Predator died
a. Was driven to extinction as well
i. Unstable cycles
ii. 20 orange universes
1. Vaseline barrier
2. Sticks with fans
a. Allowed prey mites to get away
i. Stable cycles
ii. Complex (patchy) environment 
oscillations
b. Environmental heterogeny increased stability
(cycles)

C. Optimal Foraging Strategies

 Predator max – B-C  optimal strategy


1. Bluegills eat Daphnia
 a.

D. Maintaining Species Diversity

1. Mussels and Starfish – Paine

a. Feed on prey on rocky intertied zone
b. 15 prey speices / removes starfish
i. Prey declined  15  8  1
1. Mussel MYTILUS
a. Predation of the dominant competitor
increased diversity
i. “Keystone Predator”
1. Important predator for population

E. Coevolution

 Sequence of evolutionary event in which two species modify their

interaction
o Happens when:
 Competition
 Predation
 Mutualism
 Parasitism
1. AMR
a. Anti-microbial resistance
i. Pathogens changes and makes drugs ineffective
ii. Misuse/ overuse of antibiotics  evolve resistance
1. MRSA – Meticulous streptococcus aureus
a. MCR-1: mobilized colistin resistance gene
(plasmid)
i. Bacteria – confer resistance to antibiotics
2. Myxomatosis
a. 1859  24 European rabbits brought to Australia
b. 1900s  hundred million of rabbits
i. Destroy sheep grazing land
ii. Myxoma virus was released by government – myxomatosis
– fibrosis cancer of skin
1. Vector – mosquito
c. 1950  99.8% mortality of infant rabbits
i. 75%  40%  # of days rabbits survived increased
ii. Both the rabbit and the virus changed
iii. Selection for intermediate virulent (pathogenicity)
1. How nasty the virus is
iv. Virulent strains (forms of virus)  low transmission rate
v. Avirulent forms  low transmission rates
vi. Intermediate  selected
vii. Original rabbits: 17-21 days / Field rabbits 29-36 days
1. Rabbits changed
d. 1996  rabbit hemorrhagic disease (RHD)
i. Rabbit calicivirus
ii. Transmission by direct contact
1. Did not need mosquitos anymore
2. Killed in 1-2 days
a. Rabbit populations dropped by 95%
i. Coevolutionary arms race continues
Lecture 24 – Parasitism, Immunity and
Disease
A. PARASITES - AN INTRODUCTION

 (+/-)
 Antagonistic
 Ectoparasites
o Outside the body
 Endoparasites
o Inside the body
 More than ½ living species  parasitic
 Hookworm disease – 750 million
 Schutisiners – 230 million – tremotomer
 Malaria – 230 million  600,000 people die (chills, anemia, fever)
 Ascaris – 1 billion (12% prevalence)
o 0.008 * 8 * 109  61 million died (2023)
o Zooanotic – animals to humans
o Vertebraes immune system – self from not self
 26 vaccines
o Parasites canter / evade immune system

B. MODEL OF HOST-PARASITE DYNAMICS

 SIR (susceptible/infected/resistant)
 R = avg # of new infections that 1 host gives a rise to during its life
span in a suspectable population

o
o B = transmission efficiency
o BN = # of new infections that appear
 More susceptible = more infections
 Probability of infection increases for vaccinated person in
unvaccinated person
 a + d = death rate infected individuals
 y = immunity
 Top box  getting in
 Bottom box  leaving
 Transmission to new host
 Established within host

C. TRANSMISSION ADAPTATIONS

1. Enormous Reproductive Output

 a. Schistosomes
i. Blood flat worms
ii. Schistosomiasis – 200 million people
1. Male / female  400 egg / day * 6 years = 1 million
eggs
2. Egg  miracidium  snail
3. 2000 cercaria / day * 30 day = 60,000 infected forms
4. 1 mill * 60,000 = 60 billion cercaria per adult male
and female
2. Use of Vectors
a. Agent that transmits disease organism
i. Teste fly  trypanosomes
3. Resting Stages
a. Resistant form
i. Spore, cyst, egg – withstand bad conditions
1. Parasite eggs w/ feces – ascaris
4. Behavior Modification
a. Infection can change host behavior to increase probability of
transmissablily
b. Intermediate hosts (larval)  increase predation
i. Disraelian diradical – sheep liver fluke

ii. Neural ganglia  negatively geotropic  grass

iii. Spatial / temporal overlap
c. Toxoplasma – cats are definitive host
i. Humans – cat feces
ii. Rats – intermediate hosts
1. Rats lose aversion to cat orders (attractive)
5. Timing Infective Stages Release
a. Schistosome cercariae (from snails)
i. Mid-day – increase transmission
b. Rabbit flees
 i. Don’t reproduce until they feed on blood of pregnant
rabbits
1. Want kids to be on new hosts
6. Latency/Reduced Virulence
a. Ability to produce pathogenetic effects
i. Myxoma virus – intermediate virulence – increased
transmission

D. ESTABLISHMENT ADAPTATIONS

1. Mimicry
a. Schistosomes (adult) – able to mask themselves with host
antigens  fool immune system
2. Hit and Run
a. Stimulates immune system but recovers to safer system in body
i. Larva  liver  heart  lungs
3. Live in the Immune System
a. Live in immune system
i. Toxoplasma (microphages)
ii. Mycobacterium tuberculosis (macrophages)
1. Latent TB – 2 billion people
2. Over 8 million TB cases last year
a. 2023 new cases
b. 1.25 million died
4. Antigenic Variation
a. Trypanosomes
b. Change surface antigen at regular intervals
c. VSG – (variant surface glycoprotein) cover parasite
i. VSG1  VSG2  VSG3
ii. Express different genes at different times to stay ahead of
system
Lecture 25 – Birds and the Bees and the Virus
A. THE VIRUS – HIV

 Aids – acquired immunodeficiency syndrome – HIV

o 1981 – retrovirus (347)
 DNA – double stranded / single stranded
 RNA – double stranded / single stranded
 Retrovirus – single stranded RNA  DNA
 Attach to cell  RNA 
 reverse transcriptase RNA  cDNA
 cDNA  nucleus (provirus)
 assemble  bud off
 T Helper cells (CD4 cells)
 Virus – gp120 – CD4 cells
 Destroy CD4 cells over time (antibody production)
 HIV infected  antibodies against virus, but can’t get
provirus


B. THE DISEASE - AIDS

 Destruction T helper cells  suppressed immune system

o Opportunistic infections (OI)
 Aids makes patient’s immune system bad and other
infections kill them
 Latent TB (LTBI)  latent TB  1 in 3 aids patients die from TB
 Pneumocystis (fungus)
o Common death of aids patients
 OI + HIV  HIV infection (stage 3) = AIDS
o CD4 cell count under 200
 Usually 500-1500 cells
 Mild mononucleosis  fever/rash/swollen glands
o Systems appear
 Parasite stay latent for 5-10 years
 HIV+  aids


 Treatment – vaccines
o RT  not accurate  defective copies of virus
o Variability – vaccines didn’t work
o 1-10 trillion HIV particles – HIV variants
 Excessive genetic diversity (HIV) + nucleus
 Drugs – no cure
 30 anti-HIV drugs
1. Nucleoside RT inhibitors
i. Non-nucleoside
ii. Trick RT  terminating synthesis early
1. Drug resistance was common
a. Drug A  1 in 100,000
b. Drug B  1 in 100,00
i. Both 1 in 10 billion (multiply them)
2. Protease inhibitor – late life cycle
i. Virus  becomes non-infectious
3. Fusion inhibitor
i. Prevent HIV from entering cell
4. Integrace inhibitor
i. Block inserts viral DNA from going into nucleus
 Cocktail of drugs  1 pill (3 anti-virial drugs)
 o AIDS  death sentence  chronic disease  increased death
rate
o HIV +
 Pre-expose prophylaxis (PrEP) – uninfected at risk

5.

C. PREVALENCE

 1981 – Aids  1.4 million cases

o Death rate has dropped
 18,489 deaths of aids in US (last year)
o Anti-retroviral therapy  ART
 New HIV infection 31,800 (2022)
o Transmission:
 about 80% male homosexuals (MSM)
 IV drug users or both
 Heterosexual transmission about 22% in US
 12347 people HIV+ in Indiana
 2 HIV testing sites
o Tippecanoe Health
o Planned parenthood
o HIV + 1.2 million in US
 14% don’t know
 Epidemic out of control – 15% adults HIV + in aferica
o Heterosexual transmission is common
o 40 million HIV+
o 1.3 million – neo infections
o 630,00 deaths from aids
 
 About 30 million – receiving ART – suppress virus –
suppress transmission  PEPFAR

D. TRANSMISSION

 13-24 has <1% AIDS

 About 20% new HIV infections
o SAT / HIV test
1. Delay development of antibody
2. Discrimination
a. OraQuick inhume $40
b. Everlywell $70
 Transmitted by: semen/blood/cervical secretions -- NOT
saliva/tears/sweat/urine
1. Sex
2. Exposure to blood
3. Birth
i. HIV+ moms – get tested
1. Take drugs  NRTI during pregnancy
 Behavior

E. PREVENTION

1. Abstinence
2. Be faithful  mutually monogamous
3. Condoms
a. Know partner
b. Reduce STI
UNIT
4
Lecture 28 – Behavioral Ecology
A. ETHOLOGY – mechanisms of behavior
a. Behavior ecology – evolution
b. Behavioral is adaptive  shaped by natural selection
B. COST/BENEFIT
a. Cost: energetic (ATP) cost, risk of predation, opportunity cost
b. Benefits: increased survival, increased reproductive success
(fitness)
c. B>C eggshell removal by black headed gulls
i. Advantage: Decreased predation on kids
1. Tradeoff through natural selection that maximized
the number of offspring that make it to next
generation
C. STIMULUS  RESPONSE (fix action pattern)
 Portion of stimuli evoke response  sign stimuli (releaser)
1. Sign Stimuli
a. Examples:
i. Sticklebacks – red bellies of mates

1.
ii. Ground mating birds – geese  rotate eggs  fall out of
nest  roll eggs back in
iii. Chicks responding differently to same shape “flown”

above
 iv. Chemical signals – odors from pheromones  trigger
behavior
1. Female insects release small molecules that
release downwind to attract males

2. Complex Interactions

a.
b. Steps occur in definite order
i. Behavior (mating)
ii. Courtship displays – reproductive isolating mechanism
(RIMS)
D. INNATE vs. LEARNED
 Innate – genetically induced behavior fixed for life
 Learned – environment induced behavior which can be modified


1. Evidence for a Strong Genetic Component
a. Maze-running in rats
i. Parental generation had a normal distribution of errors
ii. Bright F X Bright M and Dull F X Dull M

1. Strong genetic basis for maze running

b. Killer bees X Italian Bees
i. Wanted to get a mild manor but good pollinator
1. African Killer Bees: Brazil (1956)  US (1990)
Mississippi (1999)
a. Strong defense behaviors
i. Defensive gene where the aggressive
allele was dominant
1. Cross didn’t work well
2. Evidence for a Strong Learning Component
a. Write crown sparrows
i. Raise a male in isolation from sound  no normal song
(200 days)
ii. Male hears song (10-50 days)  normal song
1. Learned behavior
 a. Learning is selective
b. Fruit flies
i. Chemical O (mild electric shock)
ii. Chemical M (no shock)
1. 90% go to M
a. Learned behavior
i. Choose the better one for themselves
E. LEARNING AND BEHAVIOR
a. Imprinting – exposure to stimulus at particular age (critical
period) without reward or punishment
i. Ducks follow dog thinking its mom
ii. babies recognize parents face
b. Habituation – ignore persistent stimuli without reward or
punishment  filtering out insignificant stimuli
i. Listening to gossip instead of teacher
c. Classical conditioning (conditional reflex) – link 2 or more stimuli
with reward or punishments
i. Pavlou’s dog

ii.
d. Operant Conditioning (trial and error learning) – mistakes are
punished, and correct responses are rewarded (learn by doing)
e. Special learning – store information for later use
i. Know where exits are without looking
ii. Wasps fly up and circle around
1. Things are moved around, and wasps are confused
iii. Insight learning – adapt easy to new stimulus
1. Dog with leash ties themselves around a tree and
becomes stuck
a. Other dogs can remove themselves
F. Advantage / disadvantage
i. Instinct
1. Advantage – no past experience required(“perfect”
response)
a. Pre-package response to predictable event
2. Disadvantage
a. Response given to wrong stimulus
i. Motion sickness – sense send conflicting
information to brain
1. Stimulate disorientation such as
poison and makes one throw up
ii. Learning
1. Advantage: responses to unpredictable stimulus
a. Change with experience
2. Disadvantage: more complex neural circuity
a. Ample room for mistakes
iii. Bottom line
1. Inheritance defines the limits within which learning
can occur

2.
b. Gene expression is influenced by environmental experiences
Lecture 29 – Social Behavior
A. WHY FORM GROUPS?
 Group: set of conspecifics that remain together for a while and
potentially interact
 N.S. B>C for individual
1. Costs (Automatic)
a. Increased competition for: food / mates / nesting sites
b. Increased disease transmission
i. Two possible costs:
1. Risk of exploitation of parental care
a. Elephant seals (F)  1 pup / year
i. Produce good milk  525 lbs. in 4
weeks
b. Elephant Seals (M)  steal milk from
mothers
2. Risk conspecifics kill offspring (black headed gulls)
2. Benefits
a. Predator defense
i. Help defend each other
b. Improve foraging efficiency
i. Hunt / gather
c. Improve defense of resources
i. Protect resources together
d. Improve care of young
i. Aid each other in helping with offspring
B. GROUPS AS ANTI-PREDATOR MECHANISMS
1. Passive Defense
a. Predict uniformity in: size, color, behavior
i. Birds and fish form large groups
1. Effect of diffusion
2. Improved Predator Detection
a. Increase vigilance (keeping careful watch for possible danger
or difficulties) overall
i. Decreased individual vigilance
1. Prairie dogs  alarm calls to alert of predator
a. Live near relatives
3. Random Dispersal
a. Antelope uses to deal with lions
i. Cross-cross Infront of lions
4. Active Defense
a. Repeal predator
 i. Musk oxen – “circle the wagons”
1. Predation intensity is high  groups form
2. Predation intensity is low  disband (don’t hang
out)
5. Humans
a. Anti-predation response – group together
 Groups can form in response to common threat
C. GROUPS TO IMPROVE FORAGING EFFICIENCY
1. Large Prey
a. Predator forms groups for cooperative hunting
i. Amount per captured / individual is greater in groups
2. Information Centers
a. Prey- scattered / unpredictable / big
i. Roost at night and transmit info about prey
1. Ospreys: make sounds to alert of prey / resources
a. Vocalizes about food
D. GROUPS USING LOCALIZED RESOURCES
 Scare / limited
o Seals – breed on beaches – limited locations
E. WHY SHOULD SOCIAL BEHAVIOR EVOLVE?
a. Enhance original benefit of group living
b. Reproductive competition
F. “THE BATTLE OF THE SEXES”
 Females – fewer / larger gametes / invest more
 Males – many / smaller gametes / invest less


1. Sexual Selection
a. Males – flashier  increase chances of mating, decreases
chances of surviving
b. Intrasexual selection = males competition
i. Males fight  territory
c. Intersexual selection = female mate choice
i. Signals of high quality
ii. Direct – nest site / food / good territory
iii. Indirect – good genes for offspring
G. ALTRUISM
 Behavior that seems to cost the doer
 # young  measure of fitness (reproductive success)
 Individuals that help others reproduce?
1. Kin Selection
a. Directly by producing kids = individual fitness
b. Indirectly helping relative = kin selection
i. Individual fitness + kin selection = inducive fitness
2. Eusociality
a. Social system of bees / wasps/ ants/ termites
i. Most individuals are sterile (don’t reproduce)
ii. Males – unfertilized eggs  haploid
iii. Females – fertilized eggs  diploid
1. Sisters  look like dad
a. 50% like queen
i. Sisters are 75% related to each other
1. Inducive fitness
Community Ecology and Conservation Biology
Community: A group of interaction populations inhabiting a given area

1. Species richness: the number of species in a habitat

2. Species evenness: the relative abundance of species in a habitat

Together, richness and evenness make up the diversity of a community

Biodiversity On Earth

 4 species of giraffes

Global Patterns of Biodiversity in the tropics

 Temperatures affect the amounts of different animals

 Higher diversity in tropics
o Higher temps

Endemic species

 Limited geographic range

 Often found in biodiversity species
o Brown mouse lemur
o Radiated tortoise

Island biogeography:

 Biodiversity of an island is a function of immigration and extinction

rates
 Immigration
o Higher immigration rates for islands near mainland; lower
immigration rates for islands far from mainland
 Extinction
 o Smaller islands have higher extinction rates; larger islands have
lower extinction rates

Disturbance and biodiversity

o Disturbance: the total or partial disruption of communities

o Can be natural or anthropogenic
o Succession
o Primary: New habitat is created
o Secondary: Community is disturbed but new habitat is not
formed

Conservation Biology

o Applied scientific discipline devoted to protecting and managing

earth’s biodiversity
o Guided by:
o Evolution
o Ecological world
o Humans are a part of ecosystems

Why does biodiversity matter

o Threatens ecosystems
o Humans depend on other species for food, fiber, medicine

Closer to equator = more species

Why are we losing biodiversity?

o Habitat loss and degradation

o Climate change
o Pollution
o Overexploitation
o Invasive species
o 6500 invasive species in the United States alone

How do we protect biodiversity

o Protect land
o Renew and restore habitats
o Trade regulations
o Ban wildlife tracking
o Combat invasives
 o 61% of invasive species are easily available

Lecture 30 – Ecosystems

A. INTRODUCTION

1. Most inclusive
2. Self-sufficient / desert/ lake
a. Energy flow Nutrient Cycling

B. TROPHIC LEVELS AND FOOD WEBS

 Food Chain
o Autotrophic organisms
 Green plants – primary producers
 Take light from the sun and turn it into energy
(Photosynthesis)
o Herbivore – Primary consumers
 o Carnivores  secondary consumers
o Carnivores  tertiary consumers
o Decomposers  (detrivores)
 Food web – complete set of food links in community

C. ENERGY FLOW

 Rate light e  chemical e

 Gross primary productivity (GPP)
 NPP (Net primary productivity) = GPP – RSP
o Energy available

D. LAWS OF THERMODYNAMICS

1. First
a. Energy sored or used for work
i. GPP = NPP + RSP
1. (Stored) (Work)
2. Second
a. Disorder (entropy) increased in isolated systems
i. RSP cost for maintaining order
3. Application to Ecosystems
a. Producers set a spending limit on the ecosystem budget
b. Lose 90% energy in each transfer
c. Limit to the number of trophic levels
i. Food chain length limited by inefficiency of energy transfer

E. BIOMASS – Pyramid shape (less and less biomass as you go up)

 Total weight of organisms (dry weight of organic material)

o US citizens eat about 2000 pounds of food
o 70% grain  livestock
 Why not?
o Animal protein – all essential amino acids
o Plant protein

F. BIOLOGICAL MAGNIFICATION

 Increase in concentration of a chemical as you move up the trophic

level
 Larger biomass  less biomass 
 High concentration of DDT  in fish easting birds
 DDT was banned in US
 o 1973 Bald eagles had 417 nesting pairs
o 1999 5800 nesting pairs
o Today 71000 nesting pairs
 Stockholm convention  Persistent organic pollutants (POPs)
o 2001 Dirty dozen banned
 DDT was one
1. Linked chancer
2. Resistant to degrading
3. Long range transmission
4. Accumulate in living organisms
 2021 PFAS  29 chemicals were banned