Spermatogenesis

Spermatogenesis is the process by which

haploid spermatozoa develop from germ
cells in the seminiferous tubules of the
testis. This process starts with the mitotic
division of the stem cells located close to
the basement membrane of the tubules.[1]
These cells are called spermatogonial
stem cells. The mitotic division of these
produces two types of cells. Type A cells
replenish the stem cells, and type B cells
differentiate into primary spermatocytes.
The primary spermatocyte divides
meiotically (Meiosis I) into two secondary
spermatocytes; each secondary
spermatocyte divides into two equal
haploid spermatids by Meiosis II. The
spermatids are transformed into
spermatozoa (sperm) by the process of
spermiogenesis. These develop into
mature spermatozoa, also known as
sperm cells.[2] Thus, the primary
spermatocyte gives rise to two cells, the
secondary spermatocytes, and the two
secondary spermatocytes by their
subdivision produce four spermatozoa and
four haploid cells.[3]
 Spermatogenesis

Seminiferous tubule with maturing sperm.

H&E stain.

A mature human Spermatozoon

Identifiers

MeSH D013091 (https://mes

hb.nlm.nih.gov/recor
d/ui?ui=D013091)

Anatomical terminology
 Normal spermatogenesis, testis
biopsy.

High-power view of a seminiferous

tubule with normal spermatogenesis.

Spermatozoa are the mature male

gametes in many sexually reproducing
organisms. Thus, spermatogenesis is the
male version of gametogenesis, of which
the female equivalent is oogenesis. In
mammals it occurs in the seminiferous
tubules of the male testes in a stepwise
fashion. Spermatogenesis is highly
dependent upon optimal conditions for the
process to occur correctly, and is essential
for sexual reproduction. DNA methylation
and histone modification have been
implicated in the regulation of this
process.[4] It starts during puberty and
usually continues uninterrupted until
death, although a slight decrease can be
discerned in the quantity of produced
sperm with increase in age (see Male
infertility).

Spermatogenesis starts in the bottom part

of seminiferous tubes and, progressively,
cells go deeper into tubes and moving
along it until mature spermatozoa reaches
the lumen, where mature spermatozoa are
deposited. The division happens
asynchronically; if the tube is cut
transversally one could observe different
maturation states. A group of cells with
different maturation states that are being
generated at the same time is called a
spermatogenic wave.[5]

Purpose
Spermatogenesis produces mature male
gametes, commonly called sperm but
more specifically known as spermatozoa,
which are able to fertilize the counterpart
female gamete, the oocyte, during
conception to produce a single-celled
individual known as a zygote. This is the
cornerstone of sexual reproduction and
involves the two gametes both
contributing half the normal set of
chromosomes (haploid) to result in a
chromosomally normal (diploid) zygote.

To preserve the number of chromosomes

in the offspring – which differs between
species – one of each gamete must have
half the usual number of chromosomes
present in other body cells. Otherwise, the
offspring will have twice the normal
number of chromosomes, and serious
abnormalities may result. In humans,
chromosomal abnormalities arising from
incorrect spermatogenesis results in
congenital defects and abnormal birth
defects (Down syndrome, Klinefelter
syndrome) and in most cases,
spontaneous abortion of the developing
foetus.

Location in humans
Spermatogenesis takes place within
several structures of the male reproductive
system. The initial stages occur within the
testes and progress to the epididymis
where the developing gametes mature and
are stored until ejaculation. The
seminiferous tubules of the testes are the
starting point for the process, where
spermatogonial stem cells adjacent to the
inner tubule wall divide in a centripetal
direction—beginning at the walls and
proceeding into the innermost part, or
lumen—to produce immature sperm.[2]
Maturation occurs in the epididymis. The
location [Testes/Scrotum] is specifically
important as the process of
spermatogenesis requires a lower
temperature to produce viable sperm,
specifically 1°-8 °C lower than normal body
temperature of 37 °C (98.6 °F).[6] Clinically,
small fluctuations in temperature such as
from an athletic support strap, causes no
impairment in sperm viability or count.[7]

Duration
For humans, the entire process of
spermatogenesis is variously estimated as
taking 74 days[8][9] (according to tritium-
labelled biopsies) and approximately 120
days[10] (according to DNA clock
measurements). Including the transport on
ductal system, it takes 3 months. Testes
produce 200 to 300 million spermatozoa
daily.[11] However, only about half or 100
million of these become viable sperm.[12]
Stages
The entire process of spermatogenesis
can be broken up into several distinct
stages, each corresponding to a particular
type of cell in humans. In the following
table, ploidy, copy number and
chromosome/chromatid counts are for
one cell, generally prior to DNA synthesis
and division (in G1 if applicable). The
primary spermatocyte is arrested after
DNA synthesis and prior to division.
 DNA copy
ploidy/chromosomes Process entered by
Cell type number/chromatids in
in human cell
human

spermatogonium spermatocytogenesis
diploid (2N) / 46 2C / 46
(types Ad, Ap and B) (mitosis)

spermatidogenesis
primary spermatocyte diploid (2N) / 46 4C / 2x46
(meiosis I)

two secondary spermatidogenesis

haploid (N) / 23 2C / 2x23
spermatocytes (meiosis II)

four spermatids haploid (N) / 23 C / 23 spermiogenesis

four functional
haploid (N) / 23 C / 23 spermiation
spermatozoids

Spermatocytogenesis

The process of spermatogenesis as the cells progress from primary spermatocytes, to

secondary spermatocytes, to spermatids, to Sperm
 Cycle of the seminiferous epithelium
of the testis

Spermatocytogenesis is the male form of

gametocytogenesis and results in the
formation of spermatocytes possessing
half the normal complement of genetic
material. In spermatocytogenesis, a
diploid spermatogonium, which resides in
the basal compartment of the
seminiferous tubules, divides mitotically,
producing two diploid intermediate cells
called primary spermatocytes. Each
primary spermatocyte then moves into the
adluminal compartment of the
seminiferous tubules and duplicates its
DNA and subsequently undergoes meiosis
I to produce two haploid secondary
spermatocytes, which will later divide once
more into haploid spermatids. This
division implicates sources of genetic
variation, such as random inclusion of
either parental chromosomes, and
chromosomal crossover that increases the
genetic variability of the gamete. The DNA
damage response (DDR) machinery plays
an important role in spermatogenesis. The
protein FMRP binds to meiotic
chromosomes and regulates the dynamics
of the DDR machinery during
spermatogenesis.[13] FMRP appears to be
necessary for the repair of DNA damage.

Each cell division from a spermatogonium

to a spermatid is incomplete; the cells
remain connected to one another by
bridges of cytoplasm to allow
synchronous development. Not all
spermatogonia divide to produce
spermatocytes; otherwise, the supply of
spermatogonia would run out. Instead,
spermatogonial stem cells divide
mitotically to produce copies of
themselves, ensuring a constant supply of
spermatogonia to fuel
spermatogenesis.[14]
Spermatidogenesis

Spermatidogenesis is the creation of

spermatids from secondary
spermatocytes. Secondary spermatocytes
produced earlier rapidly enter meiosis II
and divide to produce haploid spermatids.
The brevity of this stage means that
secondary spermatocytes are rarely seen
in histological studies.

Spermiogenesis

During spermiogenesis, the spermatids

begin to form a tail by growing
microtubules on one of the centrioles,
which turns into basal body. These
microtubules form an axoneme. Later the
centriole is modified in the process of
centrosome reduction.[15] The anterior part
of the tail (called midpiece) thickens
because mitochondria are arranged
around the axoneme to ensure energy
supply. Spermatid DNA also undergoes
packaging, becoming highly condensed.
The DNA is packaged firstly with specific
nuclear basic proteins, which are
subsequently replaced with protamines
during spermatid elongation. The resultant
tightly packed chromatin is
transcriptionally inactive. The Golgi
apparatus surrounds the now condensed
nucleus, becoming the acrosome.

Maturation then takes place under the

influence of testosterone, which removes
the remaining unnecessary cytoplasm and
organelles. The excess cytoplasm, known
as residual bodies, is phagocytosed by
surrounding Sertoli cells in the testes. The
resulting spermatozoa are now mature but
lack motility. The mature spermatozoa are
released from the protective Sertoli cells
into the lumen of the seminiferous tubule
in a process called spermiation.
The non-motile spermatozoa are
transported to the epididymis in testicular
fluid secreted by the Sertoli cells with the
aid of peristaltic contraction. While in the
epididymis the spermatozoa gain motility
and become capable of fertilization.
However, transport of the mature
spermatozoa through the remainder of the
male reproductive system is achieved via
muscle contraction rather than the
spermatozoon's recently acquired motility.

Role of Sertoli cells

 Labelled diagram of the organisation of
Sertoli cells (red) and spermatocytes (blue)
in the testis. Spermatids which have not
yet undergone spermiation are attached to
the lumenal apex of the cell

At all stages of differentiation, the

spermatogenic cells are in close contact
with Sertoli cells which are thought to
provide structural and metabolic support
to the developing sperm cells. A single
Sertoli cell extends from the basement
membrane to the lumen of the
seminiferous tubule, although the
cytoplasmic processes are difficult to
distinguish at the light microscopic level.
Sertoli cells serve a number of functions
during spermatogenesis, they support the
developing gametes in the following ways:

Maintain the environment necessary for

development and maturation, via the
blood-testis barrier
Secrete substances initiating meiosis
Secrete supporting testicular fluid
Secrete androgen-binding protein (ABP),
which concentrates testosterone in
close proximity to the developing
gametes
Testosterone is needed in very high
quantities for maintenance of the
 reproductive tract, and ABP allows a
much higher level of fertility
Secrete hormones affecting pituitary
gland control of spermatogenesis,
particularly the polypeptide hormone,
inhibin
Phagocytose residual cytoplasm left
over from spermiogenesis
Secretion of anti-Müllerian hormone
causes deterioration of the Müllerian
duct[16]
Protect spermatids from the immune
system of the male, via the blood-testis
barrier
 Contribute to the spermatogonial stem
cell niche

The intercellular adhesion molecules

ICAM-1 and soluble ICAM-1 have
antagonistic effects on the tight junctions
forming the blood-testis barrier.[17] ICAM-2
molecules regulate spermatid adhesion on
the apical side of the barrier (towards the
lumen).[17]

Influencing factors
The process of spermatogenesis is highly
sensitive to fluctuations in the
environment, particularly hormones and
temperature. Testosterone is required in
large local concentrations to maintain the
process, which is achieved via the binding
of testosterone by androgen binding
protein present in the seminiferous
tubules. Testosterone is produced by
interstitial cells, also known as Leydig
cells, which reside adjacent to the
seminiferous tubules.

Seminiferous epithelium is sensitive to

elevated temperature in humans and some
other species, and will be adversely
affected by temperatures as high as
normal body temperature. In addition,
spermatogonia do not achieve maturity at
body temperature in most of mammals, as
β-polimerase and spermatogenic
recombinase need a specific optimal
temperature.[18] Consequently, the testes
are located outside the body in a sack of
skin called the scrotum. The optimal
temperature is maintained at 2 °C (man)
(8 °C mouse) below body temperature.
This is achieved by regulation of blood
flow[19] and positioning towards and away
from the heat of the body by the
cremasteric muscle and the dartos
smooth muscle in the scrotum.

One important mechanism is a thermal

exchange between testicular arterial and
venous blood streams. Specialized
anatomic arrangements consist of two
zones of coiling along the internal
spermatic artery. This anatomic
arrangement prolongs the time of contact
and the thermal exchange between the
testicular arterial and venous blood
streams and may, in part, explain the
temperature gradient between aortic and
testicular arterial blood reported in dogs
and rams. Moreover, reduction in pulse
pressure, occurring in the proximal one
third of the coiled length of the internal
spermatic artery.[20][21] Moreover, the
activity of spermatogenic recombinase
decreases, and this is supposed to be an
important factor of testicles
degeneration.[22]

Dietary deficiencies (such as vitamins B, E

and A), anabolic steroids, metals
(cadmium and lead), x-ray exposure,
dioxin, alcohol, and infectious diseases
will also adversely affect the rate of
spermatogenesis.[23] In addition, the male
germ line is susceptible to DNA damage
caused by oxidative stress, and this
damage likely has a significant impact on
fertilization and pregnancy.[24] Exposure to
pesticides also affects
spermatogenesis.[25]
Hormonal control
Hormonal control of spermatogenesis
varies among species. In humans the
mechanism is not completely understood;
however it is known that initiation of
spermatogenesis occurs at puberty due to
the interaction of the hypothalamus,
pituitary gland and Leydig cells. If the
pituitary gland is removed,
spermatogenesis can still be initiated by
follicle stimulating hormone (FSH) and
testosterone.[26] In contrast to FSH,
luteinizing hormone (LH) appears to have
little role in spermatogenesis outside of
inducing gonadal testosterone
production.[26][27]

FSH stimulates both the production of

androgen binding protein (ABP) by Sertoli
cells, and the formation of the blood-testis
barrier. ABP is essential to concentrating
testosterone in levels high enough to
initiate and maintain spermatogenesis.
Intratesticular testosterone levels are 20–
100 or 50–200 times higher than the
concentration found in blood, although
there is variation over a 5- to 10-fold range
amongst healthy men.[28][29] Testosterone
production does not remain constant
throughout the day, but follows a circadian
rhythm. The maximum peak of
testosterone occurs at 8 a.m., which
explains why men frequently suffer from
morning erections. In younger men,
testosterone peaks are higher.</ref> FSH
may initiate the sequestering of
testosterone in the testes, but once
developed only testosterone is required to
maintain spermatogenesis.[26] However,
increasing the levels of FSH will increase
the production of spermatozoa by
preventing the apoptosis of type A
spermatogonia. The hormone inhibin acts
to decrease the levels of FSH. Studies
from rodent models suggest that
gonadotropins (both LH and FSH) support
the process of spermatogenesis by
suppressing the proapoptotic signals and
therefore promote spermatogenic cell
survival.[30]

The Sertoli cells themselves mediate parts

of spermatogenesis through hormone
production. They are capable of producing
the hormones estradiol and inhibin. The
Leydig cells are also capable of producing
estradiol in addition to their main product
testosterone. Estrogen has been found to
be essential for spermatogenesis in
animals.[31][32] However, a man with
estrogen insensitivity syndrome (a
defective ERα) was found produce sperm
with a normal sperm count, albeit
abnormally low sperm viability; whether he
was sterile or not is unclear.[33] Levels of
estrogen that are too high can be
detrimental to spermatogenesis due to
suppression of gonadotropin secretion
and by extension intratesticular
testosterone production.[34] Prolactin also
appears to be important for
spermatogenesis.[27]

Disorders
Disorders of spermatogenesis may cause
oligospermia, which is semen with a low
concentration of sperm[35] and is a
common finding in male infertility.

See also
Anisogamy
Evolution of sexual reproduction
Folliculogenesis
Germ cells
Male infertility
Meiosis
Oncofertility
Oogenesis
Origin and function of meiosis
Sertoli cells
 Sexual reproduction
Semen analysis

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Amartya; Dighe, Rajan R. (2007). "Insights
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The McGraw-Hill Companies

Further reading
 g
Okano, Tsukasa; Ishiniwa, Hiroko;
Onuma, Manabu; Shindo, Junji;
Yokohata, Yasushi; Tamaoki, Masanori
(23 March 2016). "Effects of
environmental radiation on testes and
spermatogenesis in wild large Japanese
field mice ( Apodemus speciosus ) from
Fukushima" (https://www.ncbi.nlm.nih.g
ov/pmc/articles/PMC4804236) .
Scientific Reports. 6 (1): 23601.
Bibcode:2016NatSR...623601O (https://
ui.adsabs.harvard.edu/abs/2016NatS
R...623601O) . doi:10.1038/srep23601
(https://doi.org/10.1038%2Fsrep2360
1) . PMC 4804236 (https://www.ncbi.nl
m.nih.gov/pmc/articles/PMC4804236) .
PMID 27005329 (https://pubmed.ncbi.nl
m.nih.gov/27005329) .
Johnson, L.; Blanchard, T.L.; Varner, D.D.;
Scrutchfield, W.L. (November 1997).
"Factors affecting spermatogenesis in
the stallion". Theriogenology. 48 (7):
1199–1216. doi:10.1016/s0093-
691x(97)00353-1 (https://doi.org/10.10
16%2Fs0093-691x%2897%2900353-1) .
PMID 16728209 (https://pubmed.ncbi.nl
m.nih.gov/16728209) .
Bardin, C.W. (1991). "Pituitary-testicular
axis". In Yen, S.S.C.; Jaffee, R.B. (eds.).
Reproductive Endocrinology (3rd ed.).
Philadelphia: WB Saunders.
ISBN 0721632068.
Chambers, Christopher V.; Shafer, Mary-
Ann; Adger, Hoover; Ohm-Smith, Marilyn;
Millstein, Susan G.; Irwin, Charles E.;
Schachter, Julius; Sweet, Richard
(February 1987). "Microflora of the
urethra in adolescent boys:
Relationships to sexual activity and
nongonococcal urethritis". The Journal
of Pediatrics. 110 (2): 314–321.
doi:10.1016/s0022-3476(87)80180-4 (ht
tps://doi.org/10.1016%2Fs0022-3476%2
887%2980180-4) . PMID 3100755 (http
s://pubmed.ncbi.nlm.nih.gov/3100755)
.
Czyba, J.C.; Girod, C. (1980).
"Development of normal testis". In
Hafez, E.S.E. (ed.). Descended and
Cryptorchid Testis. The Hague: Martinus
Nijhoff. ISBN 9024723337.
Whitmore, Willet F.; Karsh, Lawrence;
Gittes, Ruben F. (October 1985). "The
Role of Germinal Epithelium and
Spermatogenesis in the Privileged
Survival of Intratesticular Grafts".
Journal of Urology. 134 (4): 782–786.
doi:10.1016/s0022-5347(17)47438-6 (ht
tps://doi.org/10.1016%2Fs0022-5347%2
 817%2947438-6) . PMID 2863395 (http
s://pubmed.ncbi.nlm.nih.gov/2863395)
.

External links
Spermatogenesis — male reproductive
physiology (http://www.health.am/sex/
more/male_infertility_spermatogenesi
s/)
Spermatogenesis animation (http://high
ered.mcgraw-hill.com/olc/dl/120112/an
im0043.swf)

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