期刊
NATURE GENETICS
卷 40, 期 6, 页码 794-799出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ng.126
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资金
- Howard Hughes Medical Institute Funding Source: Medline
- Medical Research Council [MC_U117588498] Funding Source: Medline
- NICHD NIH HHS [F32 HD052379-02, F32 HD052379, F32HD052379, HD000257] Funding Source: Medline
- Medical Research Council [MC_U117588498] Funding Source: researchfish
- MRC [MC_U117588498] Funding Source: UKRI
According to the prevailing view, mammalian X chromosomes are enriched in spermatogenesis genes expressed before meiosis(1-3) and deficient in spermatogenesis genes expressed after meiosis(2,3).The paucity of postmeiotic genes on the X chromosome has been interpreted as a consequence of meiotic sex chromosome inactivation (MSCI)-the complete silencing of genes on the XY bivalent at meiotic prophase(4,5). Recent studies have concluded that MSCI-initiated silencing persists beyond meiosis(6-8) and that most genes on the X chromosome remain repressed in round spermatids(7). Here, we report that 33 multicopy gene families, representing similar to 273 mouse X-linked genes, are expressed in the testis and that this expression is predominantly in postmeiotic cells. RNA FISH and microarray analysis show that the maintenance of X chromosome postmeiotic repression is incomplete. Furthermore, X-linked multicopy genes exhibit a similar degree of expression as autosomal genes. Thus, not only is the mouse X chromosome enriched for spermatogenesis genes functioning before meiosis, but in addition, similar to 18% of mouse X-linked genes are expressed in postmeiotic cells.
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