Spermatogenesis

Spermatogenesis is the process by which haploid spermatozoa

Spermatogenesis
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]

Spermatozoa are the mature male gametes in many sexually Seminiferous tubule with maturing
reproducing organisms. Thus, spermatogenesis is the male sperm. H&E stain.
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 A mature human Spermatozoon
methylation and histone modification have been implicated in
Identifiers
the regulation of this process.[4] It starts during puberty and
usually continues uninterrupted until death, although a slight MeSH D013091 (https://meshb.nlm.ni
decrease can be discerned in the quantity of produced sperm h.gov/record/ui?ui=D013091)
with increase in age (see Male infertility). Anatomical terminology

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]
Normal spermatogenesis, testis
biopsy.

Contents
Purpose
Location in humans
 Duration
Stages
Spermatocytogenesis
Spermatidogenesis
Spermiogenesis
Role of Sertoli cells
Influencing factors
High-power view of a seminiferous
Hormonal control tubule with normal spermatogenesis.
Disorders
See also
References
Further reading
External links

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 in Process entered by
Cell type number/chromatids in
human cell
human

spermatogonium (types spermatocytogenesis

diploid (2N) / 46 2C / 46
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

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]
Cycle of the seminiferous epithelium
FMRP appears to be necessary for the repair of DNA damage.
of the testis
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

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 Labelled diagram of the organisation of

development and maturation, via the blood-testis Sertoli cells (red) and spermatocytes
barrier (blue) in the testis. Spermatids which
Secrete substances initiating meiosis have not yet undergone spermiation are
attached to the lumenal apex of the cell
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] 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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32. Carreau S, Bouraima-Lelong H, Delalande C (2012). "Role of estrogens in
spermatogenesis". Front Biosci. 4 (1): 1–11. doi:10.2741/e356 (https://doi.org/10.2741%2Fe
356). PMID 22201851 (https://pubmed.ncbi.nlm.nih.gov/22201851).
33. Smith, Eric P.; Boyd, Jeff; Frank, Graeme R.; Takahashi, Hiroyuki; Cohen, Robert M.;
Specker, Bonny; Williams, Timothy C.; Lubahn, Dennis B.; Korach, Kenneth S. (1994).
"Estrogen Resistance Caused by a Mutation in the Estrogen-Receptor Gene in a Man". New
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at.org/issn/0028-4793). PMID 8090165 (https://pubmed.ncbi.nlm.nih.gov/8090165).
34. Edmund S. Sabanegh Jr. (20 October 2010). Male Infertility: Problems and Solutions (https://
books.google.com/books?id=YthJpK5clTMC&pg=PA83). Springer Science & Business
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Further reading
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.gov/pmc/articles/PMC4804236). Scientific Reports. 6
(1): 23601. Bibcode:2016NatSR...623601O (https://ui.adsabs.harvard.edu/abs/2016NatSR...
623601O). doi:10.1038/srep23601 (https://doi.org/10.1038%2Fsrep23601). PMC 4804236
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4804236). PMID 27005329 (https://pubmed.
ncbi.nlm.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/10.1016%2Fs0093-691x%2897%29003
53-1). PMID 16728209 (https://pubmed.ncbi.nlm.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
(https://doi.org/10.1016%2Fs0022-3476%2887%2980180-4). PMID 3100755 (https://pubme
d.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 (https://d
oi.org/10.1016%2Fs0022-5347%2817%2947438-6). PMID 2863395 (https://pubmed.ncbi.nl
m.nih.gov/2863395).

External links
Spermatogenesis — male reproductive physiology (http://www.health.am/sex/more/male_inf
ertility_spermatogenesis/)
Spermatogenesis animation (http://highered.mcgraw-hill.com/olc/dl/120112/anim0043.swf)

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