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Transcription factors SOHLH1 and SOHLH2 coordinate oocyte differentiation without affecting meiosis I.转录因子SOHLH1和SOHLH2协调卵母细胞分化,而不影响减数分裂I。
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2
Control of Meiotic Crossovers: From Double-Strand Break Formation to Designation.减数分裂交叉的控制:从双链断裂形成到指定
Annu Rev Genet. 2016 Nov 23;50:175-210. doi: 10.1146/annurev-genet-120215-035111. Epub 2016 Sep 14.
3
Use of DEAD-box polypeptide-4 (Ddx4) gene promoter-driven fluorescent reporter mice to identify mitotically active germ cells in post-natal mouse ovaries.利用DEAD盒多肽4(Ddx4)基因启动子驱动的荧光报告小鼠鉴定出生后小鼠卵巢中有丝分裂活跃的生殖细胞。
Mol Hum Reprod. 2015 Jan;21(1):58-65. doi: 10.1093/molehr/gau071. Epub 2014 Aug 21.
4
Building an ovary: insights into establishment of somatic cell lineages in the mouse.构建卵巢:对小鼠体细胞谱系建立的见解
Sex Dev. 2014;8(5):243-51. doi: 10.1159/000358072. Epub 2014 Jan 29.
5
Spermatogonial SOHLH1 nucleocytoplasmic shuttling associates with initiation of spermatogenesis in the rhesus monkey (Macaca mulatta).精原细胞 SOEH1 的核质穿梭与食蟹猴(Macaca mulatta)精子发生的启动有关。
Mol Hum Reprod. 2014 Apr;20(4):350-7. doi: 10.1093/molehr/gat093. Epub 2013 Dec 9.
6
Oocyte differentiation is genetically dissociable from meiosis in mice.卵母细胞分化在遗传上与小鼠的减数分裂分离。
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7
Follicular assembly: mechanisms of action.滤泡组装:作用机制。
Reproduction. 2012 Feb;143(2):139-49. doi: 10.1530/REP-11-0299. Epub 2011 Nov 7.
8
SOHLH1 and SOHLH2 coordinate spermatogonial differentiation.SOHLH1 和 SOHLH2 协调精原细胞分化。
Dev Biol. 2012 Jan 15;361(2):301-12. doi: 10.1016/j.ydbio.2011.10.027. Epub 2011 Oct 26.
9
Oogenesis: transcriptional regulators and mouse models.卵子发生:转录调控因子和小鼠模型。
Mol Cell Endocrinol. 2012 Jun 5;356(1-2):31-9. doi: 10.1016/j.mce.2011.07.049. Epub 2011 Aug 12.
10
Germ cell-specific transcriptional regulator sohlh2 is essential for early mouse folliculogenesis and oocyte-specific gene expression.生殖细胞特异性转录调节因子Sohlh2对小鼠早期卵泡发生和卵母细胞特异性基因表达至关重要。
Biol Reprod. 2008 Dec;79(6):1176-82. doi: 10.1095/biolreprod.108.071217. Epub 2008 Aug 27.

卵母细胞生长和存活而非减数分裂I的SO(H)L(H)“O”驱动因素。

The SO(H)L(H) "O" drivers of oocyte growth and survival but not meiosis I.

作者信息

Kumar T Rajendra

出版信息

J Clin Invest. 2017 Jun 1;127(6):2044-2047. doi: 10.1172/JCI94665. Epub 2017 May 15.

DOI:10.1172/JCI94665
PMID:28504648
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5451244/
Abstract

The spermatogenesis/oogenesis helix-loop-helix (SOHLH) proteins SOHLH1 and SOHLH2 play important roles in male and female reproduction. Although previous studies indicate that these transcriptional regulators are expressed in and have in vivo roles in postnatal ovaries, their expression and function in the embryonic ovary remain largely unknown. Because oocyte differentiation is tightly coupled with the onset of meiosis, it is of significant interest to determine how early oocyte transcription factors regulate these two processes. In this issue of the JCI, Shin and colleagues report that SOHLH1 and SOHLH2 demonstrate distinct expression patterns in the embryonic ovary and interact with each other and other oocyte-specific transcription factors to regulate oocyte differentiation. Interestingly, even though there is a rapid loss of oocytes postnatally in ovaries with combined loss of Sohlh1 and Sohlh2, meiosis is not affected and proceeds normally.

摘要

精子发生/卵子发生螺旋-环-螺旋(SOHLH)蛋白SOHLH1和SOHLH2在雄性和雌性生殖中发挥重要作用。尽管先前的研究表明这些转录调节因子在出生后的卵巢中表达并在体内发挥作用,但其在胚胎卵巢中的表达和功能仍 largely未知。由于卵母细胞分化与减数分裂的开始紧密相关,确定早期卵母细胞转录因子如何调节这两个过程具有重要意义。在本期《临床研究杂志》中,Shin及其同事报告称,SOHLH1和SOHLH2在胚胎卵巢中表现出不同的表达模式,并相互作用以及与其他卵母细胞特异性转录因子相互作用以调节卵母细胞分化。有趣的是,尽管在Sohlh1和Sohlh2联合缺失的卵巢中出生后卵母细胞会迅速丢失,但减数分裂不受影响且正常进行。