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==Spermatogenesis== [[Mammal]]ian [[spermatogenesis]] is representative for most animals. In human males, spermatogenesis begins at puberty in [[seminiferous tubules]] in the testicles and go on continuously. Spermatogonia are immature germ cells. They proliferate continuously by mitotic divisions around the outer edge of the [[seminiferous tubule]]s, next to the [[basal lamina]]. Some of these cells stop proliferation and differentiate into primary spermatocytes. After they proceed through the first meiotic division, two secondary spermatocytes are produced. The two secondary spermatocytes undergo the second meiotic division to form four haploid spermatids. These spermatids differentiate morphologically into sperm by nuclear condensation, ejection of the cytoplasm and formation of the [[acrosome]] and [[flagellum]].{{citation needed|date=December 2011}} The developing male germ cells do not complete [[cytokinesis]] during spermatogenesis. Consequently, cytoplasmic bridges exist during interphase to ensure connection between the clones of differentiating daughter cells. These bridges are called a [[syncytium]], and feature a [[TEX14]] and [[KIF23]] ring in their centre.<ref>{{cite journal | vauthors = Greenbaum MP, Yan W, Wu MH, Lin YN, Agno JE, Sharma M, Braun RE, Rajkovic A, Matzuk MM | display-authors = 6 | title = TEX14 is essential for intercellular bridges and fertility in male mice | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 103 | issue = 13 | pages = 4982–4987 | date = March 2006 | pmid = 16549803 | pmc = 1458781 | doi = 10.1073/pnas.0505123103 | bibcode = 2006PNAS..103.4982G | doi-access = free }}</ref><ref>{{cite journal | vauthors = Greenbaum MP, Iwamori N, Agno JE, Matzuk MM | title = Mouse TEX14 is required for embryonic germ cell intercellular bridges but not female fertility | journal = Biology of Reproduction | volume = 80 | issue = 3 | pages = 449–457 | date = March 2009 | pmid = 19020301 | pmc = 2805395 | doi = 10.1095/biolreprod.108.070649 }}</ref> In this way the haploid cells are supplied with all the products of a complete diploid [[genome]]. Sperm that carry a [[Y chromosome]], for example, are supplied with essential molecules that are encoded by genes on the [[X chromosome]].{{citation needed|date=December 2011}} Success of germ cell proliferation and differentiation is also ensured by a balance between germ cell development and programmed cell death. Identification of «death triggering signals» and corresponding receptor proteins is important for the fertilization potential of males. Apoptosis in germ cells can be induced by variety of naturally occurring toxicant. Receptors belonging to the taste 2 family are specialized to detect bitter compounds including extremely toxic alkaloids. So taste receptors play a functional role for controlling apoptosis in male reproductive tissue.<ref>{{cite journal | vauthors = Luddi A, Governini L, Wilmskötter D, Gudermann T, Boekhoff I, Piomboni P | title = Taste Receptors: New Players in Sperm Biology | journal = International Journal of Molecular Sciences | volume = 20 | issue = 4 | page = 967 | date = February 2019 | pmid = 30813355 | pmc = 6413048 | doi = 10.3390/ijms20040967 | doi-access = free }}</ref> ===Mutation and DNA repair=== The mutation frequencies for cells throughout the different stages of [[spermatogenesis]] in mice is similar to that in female germline cells, that is 5 to 10-fold lower than the mutation frequency in somatic cells<ref name="pmid9707592">{{cite journal | vauthors = Walter CA, Intano GW, McCarrey JR, McMahan CA, Walter RB | title = Mutation frequency declines during spermatogenesis in young mice but increases in old mice | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 95 | issue = 17 | pages = 10015–10019 | date = August 1998 | pmid = 9707592 | pmc = 21453 | doi = 10.1073/pnas.95.17.10015 | doi-access = free | bibcode = 1998PNAS...9510015W }}</ref><ref name="pmid23153565" /> Thus low mutation frequency is a feature of germline cells in both sexes. Homologous recombinational repair of double-strand breaks occurs in mouse during sequential stages of spermatogenesis, but is most prominent in [[spermatocyte]]s.<ref name="pmid9778439"/> The lower frequencies of mutation in germ cells compared to somatic cells appears to be due to more efficient removal of DNA damages by repair processes including homologous recombination repair during meiosis.<ref>Bernstein H, Byerly HC, Hopf FA, Michod RE. Genetic damage, mutation, and the evolution of sex. Science. 1985 Sep 20;229(4719):1277-81. doi: 10.1126/science.3898363. PMID 3898363</ref> Mutation frequency during spermatogenesis increases with age.<ref name="pmid9707592" /> The mutations in spermatogenic cells of old mice include an increased prevalence of [[transversion]] mutations compared to young and middle-aged mice.<ref name="pmid15084311">{{cite journal | vauthors = Walter CA, Intano GW, McMahan CA, Kelner K, McCarrey JR, Walter RB | title = Mutation spectral changes in spermatogenic cells obtained from old mice | journal = DNA Repair | volume = 3 | issue = 5 | pages = 495–504 | date = May 2004 | pmid = 15084311 | doi = 10.1016/j.dnarep.2004.01.005 }}</ref>
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