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Spermatid
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{{short description|Direct precursor of a sperm cell}} {{Infobox anatomy | Name = Spermatid | Latin = | Image = Germinal_epithelium_testicle.svg | Caption = ''Germinal epithelium of the [[testicle]].''<br>1: [[basal lamina]]<br>2: [[spermatogonia]]<br>3: [[spermatocyte]] 1st order<br>4: spermatocyte 2nd order<br>5: spermatid<br>6: mature spermatid<br>7: [[Sertoli cell]]<br>8: [[tight junction]] ([[blood testis barrier]]) | Image2 = Gray1150.png | Caption2 = Transverse section of a [[tubule]] of the [[testis]] of a [[rat]]. Γ 250. | System = }} The '''spermatid''' is the [[haploid]] male [[gametid]] that results from division of secondary [[spermatocyte]]s. As a result of [[meiosis]], each spermatid contains only half of the genetic material present in the original primary spermatocyte. Spermatids are connected by cytoplasmic material and have superfluous cytoplasmic material around their nuclei. When formed, ''early round spermatids'' must undergo further maturational events to develop into [[spermatozoa]], a process termed [[spermiogenesis]] (also termed ''spermeteliosis''). The spermatids begin to grow a living thread, develop a thickened mid-piece where the [[mitochondria]] become localised, and form an [[acrosome]]. 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. In 2016 scientists at [[Nanjing Medical University]] claimed they had produced cells resembling mouse spermatids artificially from [[stem cells]]. They injected these spermatids into mouse eggs and produced pups.<ref name="Nature">{{cite journal|last1=Cyranoski|first1=David|title=Researchers claim to have made artificial mouse sperm in a dish|journal=Nature|date=25 February 2016|doi=10.1038/nature.2016.19453|s2cid=87014225|url=http://www.nature.com/news/researchers-claim-to-have-made-artificial-mouse-sperm-in-a-dish-1.19453|access-date=4 March 2016|url-access=subscription}}</ref> During spermatid [[ploidy|haploid]] [[genome]] remodeling, the majority of [[histone]]s are replaced by [[protamine]]s, and the [[DNA]] is compacted. During this compaction, transient single- and double-strand breaks are introduced into the sperm DNA.<ref>{{cite journal |vauthors=Gouraud A, Brazeau MA, GrΓ©goire MC, Simard O, Massonneau J, Arguin M, Boissonneault G |title="Breaking news" from spermatids |journal=Basic Clin Androl |volume=23 |issue= |pages=11 |date=2013 |pmid=25780573 |pmc=4349474 |doi=10.1186/2051-4190-23-11 |doi-access=free |url=}}</ref> The conventional [[non-homologous end joining]] pathway for repairing double-strand breaks is not available for elongated spermatids. However, spermatids can carry out limited repair of exogenous and programmed double-strand breaks using an alternative error-prone non-homologous end joining repair pathway.<ref>{{cite journal |vauthors=Ahmed EA, Scherthan H, de Rooij DG |title=DNA Double Strand Break Response and Limited Repair Capacity in Mouse Elongated Spermatids |journal=Int J Mol Sci |volume=16 |issue=12 |pages=29923β35 |date=December 2015 |pmid=26694360 |pmc=4691157 |doi=10.3390/ijms161226214 |doi-access=free |url=}}</ref> If DNA strand breaks persist in mature sperm, the result can be increased sperm DNA fragmentation which is associated with impaired fertility and an increased incidence of miscarriage.<ref>{{cite journal |vauthors=Aitken RJ, De Iuliis GN |title=On the possible origins of DNA damage in human spermatozoa |journal=Mol Hum Reprod |volume=16 |issue=1 |pages=3β13 |date=January 2010 |pmid=19648152 |doi=10.1093/molehr/gap059 |url=}}</ref> ==DNA repair== As postmeiotic [[germ cell]]s develop to mature [[sperm]] they progressively lose the ability to repair [[DNA damage (naturally occurring)|DNA damage]] that may then accumulate and be transmitted to the [[zygote]] and ultimately the embryo.<ref name="pmid18282746">{{cite journal |vauthors=Marchetti F, Wyrobek AJ |title=DNA repair decline during mouse spermiogenesis results in the accumulation of heritable DNA damage |journal=DNA Repair (Amst.) |volume=7 |issue=4 |pages=572β81 |year=2008 |pmid=18282746 |doi=10.1016/j.dnarep.2007.12.011 |s2cid=1316244 |url=https://digital.library.unt.edu/ark:/67531/metadc895292/}}</ref> In particular, the [[DNA repair|repair of DNA]] double-strand breaks by the [[non-homologous end joining]] pathway, although present in round spermatids, appears to be lost as they develop into elongated spermatids.<ref>{{cite journal |vauthors=Ahmed EA, Scherthan H, de Rooij DG |title=DNA Double Strand Break Response and Limited Repair Capacity in Mouse Elongated Spermatids |journal=Int J Mol Sci |volume=16 |issue=12 |pages=29923β35 |date=December 2015 |pmid=26694360 |pmc=4691157 |doi=10.3390/ijms161226214 |doi-access=free |url=}}</ref> ==Additional images== <gallery> File:Gray's 7 (ovum maturation).svg|Scheme showing analogies in the process of maturation of the [[ovum]] and the development of the [[Genyo]] [[spermatids]] (young [[spermatozoa]]) </gallery> == See also == [[List of distinct cell types in the adult human body]] ==References== {{Reflist}} ==External links== * {{BUHistology|17804loa}} - "Male Reproductive System: testis, early spermatids" * {{BUHistology|17805loa}} - "Male Reproductive System: testis, late spermatids" * [https://web.archive.org/web/20061209185910/http://www.cvm.okstate.edu/instruction/mm_curr/histology/MR/himrp3.htm Histology at okstate.edu] {{Male reproductive system}} [[Category:Reproductive system]] [[Category:Germ cells]] [[Category:Andrology]]
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