Spermatocyte

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spermatids and to sperm
.

Spermatocytes are a type of

seminiferous tubules.[1] There are two types of spermatocytes, primary and secondary spermatocytes. Primary and secondary spermatocytes are formed through the process of spermatocytogenesis.[2]

Primary spermatocytes are

haploid (N) cells that contain half the number of chromosomes.[1]

In all animals,

hermaphrodites such as C. elegans, which exist as a male or hermaphrodite. In hermaphrodite C. elegans, sperm production occurs first and is then stored in the spermatheca. Once the eggs are formed, they are able to self-fertilize and produce up to 350 progeny.[3]

Development

spermatogonial stem cells which begin differentiation to type B spermatogonia, which have round nuclei and heterochromatin attached to the nuclear envelope and the center of nucleolus.[4] Type B cells will move on to the adluminal compartment (towards the inner region of tubule) and become primary spermatocytes; this process takes about 16 days to complete.[2][5]

The primary spermatocytes within the adluminal compartment will continue on to

meiosis II.[1]

Although spermatocytes that divide mitotically and meiotically are sensitive to

spermatogonial stem cells are not. Therefore, after termination of radiation therapy or chemotherapy, the spermatognia stems cells may re-initiate the formation of spermatogenesis.[6]

Hormones produced by the Pituitary gland. GnRH is secreted by the hypothalamus, which induces anterior pituitary to produce FSH and LH upon puberty.

Role of hormones

The formation of primary spermatocytes (a process known as

meiotic prophase.[1]

Cell type summary

In the following table, ploidy, copy number and chromosome/chromatid counts listed are for a single cell, generally prior to DNA synthesis and division (in G1 if applicable). Primary spermatocytes are arrested after DNA synthesis and prior to division.[1][2]

Cell Type Ploidy/
Chromosomes
in human		 DNA copy number/
Chromatids
in human		 Process entered by cell Duration
spermatogonium (types Ad, Ap and B)
germ cells
 diploid (2N) / 46 2C / 46 spermatocytogenesis (mitosis) 16 days
primary spermatocyte male gametocyte diploid (2N) / 46 4C / 2x46
meiosis I
)		 24 days
secondary spermatocyte male gametocyte haploid (N) / 23 2C / 46
meiosis II
)		 A few hours
spermatids male gametid haploid (N) / 23 1C / 23 spermiogenesis 24 days
spermatozoids
 sperm haploid (N) / 23 1C / 23 spermiation 64 days (total)

Physiology

Damage, repair, and failure

Spermatocytes regularly overcome double-strand breaks and other

H2AX, which recognize double strand breaks and modify chromatin, respectively. As a result, double strand breaks in meiotic cells, unlike mitotic cells, do not typically lead to apoptosis, or cell death.[9] Homologous recombinational repair (HRR) of double-strand breaks occurs in mice during sequential stages of spermatogenesis but is most prominent in spermatocytes.[10] In spermatocytes, HRR events occur mainly in the pachytene stage of meiosis and the gene conversion type of HRR is predominant, whereas in other stages of spermatogenesis the reciprocal exchange type of HRR is more frequent.[10] During mouse spermatogenesis, the mutation frequencies of cells at the different stages, including pachytene spermatocytes, are 5 to 10-fold lower than the mutation frequencies in somatic cells.[11] Because of their elevated DNA repair
capability, spermatocytes likely play a central role in the maintenance of these lower mutation rates, and thus in the preservation of the genetic integrity of the male germ line.

It is known that

H2AX presence in pachytene spermatocytes.[12]

Specific mutations

Wild-type spermatocyte progression compared to repro4 mutated spermatocytes.

The gene Stimulated By Retinoic Acid 8 (STRA8) is required for the retinoic-acid signaling pathway in humans, which leads to

leptotene spermatocytes can result in premature chromosome condensation.[13]

Mutations in Mtap2, a

meiosis I. This is observed by a reduction in spermatid presence in repro4 mutants.[14]

Recombinant-defective mutations can occur in

ATM and MSH5 genes of spermatocytes. These mutations involve double strand break repair impairment, which can result in arrest of spermatogenesis at stage IV of the seminiferous epithelium cycle.[15]

History

Meiosis in Grasshopper testes (primary spermatocytes in zygotene, pachytene, prophase I).

The

extrinsic (FSH and LH) factors.[16] The spermatogenesis process in mammals as a whole, involving cellular transformation, mitosis, and meiosis, has been well studied and documented from the 1950s to 1980s. However, during the 1990s and 2000s researchers have focused around increasing understanding of the regulation of spermatogenesis via genes, proteins, and signaling pathways, and the biochemical and molecular mechanisms involved in these processes. Most recently, the environmental effects on spermatogenesis have become a focus as male infertility in men has become more prevalent.[17]

An important discovery in the spermatogenesis process was the identification of the seminiferous epithelial cycle in mammals—work by C.P. Leblound and Y. Clermont in 1952 that studied the spermatogonia, spermatocyte layers and spermatids in rat seminiferous tubules. Another critical discovery was that of the hypothalamic-pituitary-testicular hormone chain, which plays a role in spermatogenesis regulation; this was studied by R. M. Sharpe in 1994.[17]

Other animals

centrioles independently in the G2 phase and are sensitive to microtubule-targeting drugs. Normally, primary cilia will develop from one centriole in the G0/G1 phase and are not affected by microtubule targeting drugs.[18]

chromosomes. By the end of the anaphase stage, there is one at each pole moving between the spindle poles without actually having physical interactions with one another (also known as distance segregation). These unique traits allow researchers to study the force created by the spindle poles to allow the chromosomes to move, cleavage furrow management and distance segregation.[19][20]

See also

References

  1. ^
    ISBN 978-1-4377-1753-2. {{cite book}}: |first1= has generic name (help)CS1 maint: multiple names: authors list (link)[page needed
    ]
  2. ^ a b c Schöni-Affolter, Dubuis-Grieder, Strauch, Franzisk, Christine, Erik Strauch. "Spermatogenesis". Retrieved 22 March 2014.{{cite web}}: CS1 maint: multiple names: authors list (link)
  3. ^ Riddle, DL; Blumenthal, T; Meyer, B.J.; et al., eds. (1997). "I, The Biological Model". C. elegans II (2nd ed.). Cold Spring Harbor. NY: Cold Spring Harbor Laboratory Press. Retrieved April 13, 2014.
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  5. PMID 5917196
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  6. ISBN 9780323078429.{{cite book}}: CS1 maint: multiple names: authors list (link
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  7. ISBN 9781133714071.{{cite book}}: CS1 maint: multiple names: authors list (link
    )
  8. ISBN 978-0495391845
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  9. S2CID 21185220
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  10. ^
    S2CID 24830710
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  11. PMID 9707592
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  13. PMID 18799790
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  14. PMID 24501684
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  16. ISBN 978-0-387-79990-2
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  17. ^
    PMID 20403863
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  18. PMID 24244850
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  19. S2CID 59941923
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  20. S2CID 13210761
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External links
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