Does MAX open up a new avenue for meiotic research?

Does MAX open up a new avenue for meiotic research?
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MAX是否为减数分裂研究开辟了新途径?

DOI:
10.1111/dgd.12344
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发表时间:
2017
期刊:
影响因子:
2.5
通讯作者:
A.
A.
中科院分区:
生物学4区
文献类型:
--
作者:
Suzuki;A.;Hirasaki;M.;Okuda;A.

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减数分裂是有性生殖的中心事件。与体细胞一样,生殖细胞进行有丝分裂以增加其细胞数量,但与体细胞不同的是,生殖细胞在配子发生的某个点将其细胞分裂模式从有丝分裂切换到减数分裂。然而,这种开关的分子基础仍然难以捉摸。在这篇综述文章中,我们概述了哺乳动物减数分裂的发生,包括我们最近发现MYC相关因子X(MAX)分别防止胚胎干细胞(ESCs)和生殖细胞的异位和早熟减数分裂。我们提出了一个以MAX为中心的分子网络的假设模型,该网络调节哺乳动物的减数分裂进入,并提出可诱导的Maxknockout ESCs为探索减数分裂起始的分子机制提供了一个很好的平台,同时排除了配子发生的其他方面。
Meiosis is a central event of sexual reproduction. Like somatic cells, germ cells conduct mitosis to increase their cell number, but unlike somatic cells, germ cells switch their cell division mode from mitosis to meiosis at a certain point in gametogenesis. However, the molecular basis of this switch remains elusive. In this review article, we give an overview of the onset of mammalian meiosis, including our recent finding that MYC Associated Factor X (MAX) prevents ectopic and precocious meiosis in embryonic stem cells (ESCs) and germ cells, respectively. We present a hypothetical model of a MAX‐centered molecular network that regulates meiotic entry in mammals and propose that inducibleMaxknockout ESCs provide an excellent platform for exploring the molecular mechanisms of meiosis initiation, while excluding other aspects of gametogenesis.
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