Editing Spermatogenesis (section)

=== Spermatocytogenesis ===
{{Main|Spermatocytogenesis}}
[[File:Figure 28 01 04.jpg|right|thumb|500px|The process of spermatogenesis as the cells progress from primary spermatocytes, to secondary spermatocytes, to spermatids, to Sperm]]
[[File:Seminiferous Cycle.svg|thumb|Cycle of the seminiferous epithelium of the testis]]
Spermatocytogenesis is the male form of [[gametocyte|gametocytogenesis]] and results in the formation of [[spermatocyte]]s 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 [[spermatocyte|primary spermatocyte]]s. 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 [[spermatocyte|secondary spermatocyte]]s, 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 (naturally occurring)|DNA damage]] response (DDR) machinery plays an important role in spermatogenesis.  The protein [[FMR1|FMRP]] binds to [[meiosis|meiotic chromosomes]] and regulates the dynamics of the DDR machinery during spermatogenesis.<ref name="pmid24813610">{{cite journal |vauthors=Alpatov R, Lesch BJ, Nakamoto-Kinoshita M, Blanco A, Chen S, Stützer A, Armache KJ, Simon MD, Xu C, Ali M, Murn J, Prisic S, Kutateladze TG, Vakoc CR, Min J, Kingston RE, Fischle W, Warren ST, Page DC, Shi Y |title=A chromatin-dependent role of the fragile X mental retardation protein FMRP in the DNA damage response |journal=Cell |volume=157 |issue=4 |pages=869–81 |date=May 2014 |pmid=24813610 |pmc=4038154 |doi=10.1016/j.cell.2014.03.040 }}</ref>  FMRP appears to be necessary for the [[DNA repair|repair of DNA damage]].

During spermatocytogenesis, meiosis employs special [[DNA repair]] processes that remove DNA damages and help maintain the integrity of the [[genome]] that is passed on to progeny.<ref name = Garcia-Rodriguez2018>{{cite journal |vauthors=García-Rodríguez A, Gosálvez J, Agarwal A, Roy R, Johnston S |title=DNA Damage and Repair in Human Reproductive Cells |journal=Int J Mol Sci |volume=20 |issue=1 |date=December 2018 |page=31 |pmid=30577615 |doi=10.3390/ijms20010031 |doi-access=free |pmc=6337641 |url=}}</ref>  These DNA repair processes include [[homologous recombination]]al repair and [[non-homologous end joining]]<ref name = Garcia-Rodriguez2018/>

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|spermatogonial stem cells]] divide mitotically to produce copies of themselves, ensuring a constant supply of spermatogonia to fuel spermatogenesis.<ref>{{cite journal |doi=10.1002/ar.20412 |title=Comparative spermatogenesis, spermatocytogenesis, and spermato-zeugmata formation in males of viviparous species of clinid fishes (Teleostei: Clinidae, Blennioidei) |year=2007 |last1=Fishelson |first1=Lev |last2=Gon |first2=Ofer |last3=Holdengreber |first3=Vered |last4=Delarea |first4=Yakob |journal=The Anatomical Record |volume=290 |issue=3 |pages=311–23 |pmid=17525946|s2cid=25069965 |doi-access=free }}</ref>