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MORC2B 对于减数分裂进程和生育能力是必不可少的。

MORC2B is essential for meiotic progression and fertility.

机构信息

State Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing, China.

Department of Biomedical Sciences, University of Pennsylvania School of Veterinary Medicine, Philadelphia, Pennsylvania, United States of America.

出版信息

PLoS Genet. 2018 Jan 12;14(1):e1007175. doi: 10.1371/journal.pgen.1007175. eCollection 2018 Jan.

DOI:10.1371/journal.pgen.1007175
PMID:29329290
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5785033/
Abstract

The microrchidia (MORC) family proteins are chromatin-remodelling factors and function in diverse biological processes such as DNA damage response and transposon silencing. Here, we report that mouse Morc2b encodes a functional germ cell-specific member of the MORC protein family. Morc2b arose specifically in the rodent lineage through retrotransposition of Morc2a during evolution. Inactivation of Morc2b leads to meiotic arrest and sterility in both sexes. Morc2b-deficient spermatocytes and oocytes exhibit failures in chromosomal synapsis, blockades in meiotic recombination, and increased apoptosis. Loss of MORC2B causes mis-regulated expression of meiosis-specific genes. Furthermore, we find that MORC2B interacts with MORC2A, its sequence paralogue. Our results demonstrate that Morc2b, a relatively recent gene, has evolved an essential role in meiosis and fertility.

摘要

微环 (MORC) 家族蛋白是染色质重塑因子,在多种生物学过程中发挥作用,如 DNA 损伤反应和转座子沉默。在这里,我们报告说,小鼠 Morc2b 编码了一种功能性的生殖细胞特异性 MORC 蛋白家族成员。Morc2b 是通过 Morc2a 在进化过程中的逆转座而特异性出现在啮齿动物谱系中的。Morc2b 的失活导致雌雄两性的减数分裂停滞和不育。Morc2b 缺陷的精母细胞和卵母细胞表现出染色体联会失败、减数分裂重组阻滞和凋亡增加。MORC2B 的缺失导致减数分裂特异性基因的表达失调。此外,我们发现 MORC2B 与它的序列同源物 MORC2A 相互作用。我们的结果表明,Morc2b 作为一个相对较新的基因,在减数分裂和生育能力方面进化出了至关重要的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa92/5785033/d345b7b5cd6d/pgen.1007175.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa92/5785033/51bb08682f47/pgen.1007175.g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa92/5785033/049a501193e7/pgen.1007175.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa92/5785033/f955425dcf5c/pgen.1007175.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa92/5785033/ea1bc408800d/pgen.1007175.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa92/5785033/3b71230bc592/pgen.1007175.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa92/5785033/d345b7b5cd6d/pgen.1007175.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa92/5785033/51bb08682f47/pgen.1007175.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa92/5785033/5bc234850feb/pgen.1007175.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa92/5785033/b57d42bd5185/pgen.1007175.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa92/5785033/049a501193e7/pgen.1007175.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa92/5785033/f955425dcf5c/pgen.1007175.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa92/5785033/ea1bc408800d/pgen.1007175.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa92/5785033/3b71230bc592/pgen.1007175.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa92/5785033/d345b7b5cd6d/pgen.1007175.g008.jpg

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