PRMT7 is involved in regulation of germ cell proliferation during embryonic stage

PRMT7 is involved in regulation of germ cell proliferation during embryonic stage
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DOI:
10.1016/j.bbrc.2020.09.099
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发表时间:
2020-12-17
影响因子:
3.1
通讯作者:
Gao, Fei
Gao, Fei
中科院分区:
生物学4区
文献类型:
--
作者:
Chen, Min;Wang, Yanbo;Gao, Fei

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精氨酸甲基化是蛋白质精氨酸甲基转移酶(PRMTs)催化的最重要的翻译后修饰之一。先前的研究表明,Prmt5在生殖细胞发育中起重要作用。Prmt7是唯一负责精氨酸残基单甲基化的家族成员。然而,Prmt7是否也参与生殖细胞发育尚不清楚。在本研究中,我们发现PRMT7在胚胎期(从E10.5开始)的雄性生殖细胞中大量表达。Prmt7的缺失导致胚胎期生殖细胞增殖缺陷,在E11.5时Prmt7(-/-)小鼠的原始生殖细胞数量显著减少。我们还发现P5时Prmt7(-/-)小鼠的睾丸大小减少,生殖细胞数量和精管直径减少。进一步研究发现,在E12.5时,Prmt7(-/-)小鼠生殖细胞中bmp和tgf - β单链通路的表达发生了显著变化。然而,在成年Prmt7(-/flox)中未观察到睾丸发育缺陷;Mvh-Cre老鼠。总之,本研究表明,Prmt7在胚胎阶段的男性生殖细胞增殖中起作用,而不是出生后生殖细胞发育所必需的。(C) 2020爱思唯尔公司版权所有。
Arginine methylation is one of the most important post-translational modifications which is catalyzed by protein arginine methyltransferases (PRMTs). Previous studies have demonstrated that Prmt5 plays important role in germ cell development. Prmt7 is the only family member responsible for mono-methylation of arginine residue. However, whether Prmt7 is also involved in germ cell development remains unclear. In this study, we find that PRMT7 is abundantly expressed in the male germ cells during embryonic stage (from E10.5). Depletion of Prmt7 results in the defect of germ cell proliferation during embryonic stage and the number of primordial germ cells is significantly reduced in Prmt7(-/-) mice at E11.5. We also find that the size of testes is reduced in Prmt7(-/-) mice at P5 with reduced germ cell number and the diameter of seminiferous tubules. Further study reveals that the expression of BMPs and TGF-beta singling pathway is significantly changed in germ cells of Prmt7(-/-) mice at E12.5. However, no defect of testes development is observed in adult Prmt7(-/flox); Mvh-Cre mice. Collectively, this study demonstrates that Prmt7 plays roles in male germ cell proliferation during embryonic stages and it is not required for germ cell development postnatally. (C) 2020 Elsevier Inc. All rights reserved.