A twist of fate: How a meiotic protein is providing new perspectives on germ cell development.
A twist of fate: How a meiotic protein is providing new perspectives on germ cell development.
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命运的转折：减数分裂蛋白如何为生殖细胞发育提供新的视角。
DOI：
10.1080/21624054.2016.1175259
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发表时间：
2016
期刊：
影响因子：
--
通讯作者：
Yanowitz,JudithL
中科院分区：
文献类型：
--
作者：
Mainpal,Rana;Yanowitz,JudithL
控制生殖细胞命运的分子途径是一个深入研究的领域，对辅助生殖技术的发展、不孕症干预和生殖细胞癌的治疗具有重要意义。转录抑制已成为确保抑制原始生殖细胞体细胞生长程序的主要机制。在这篇评论中，我们地址howxnd-1阐明了我们的理解转录抑制，以及它是如何与生殖细胞分化程序相协调。我们最近发现xnd-1是秀丽隐杆线虫生殖细胞命运的一个新的早期决定因素。我们的研究表明，XND-1是母体沉积到早期胚胎中，在那里它选择性地富集在生殖谱系中，然后在整个发育过程中只在生殖谱系中的染色质上发现，当它在粗线期晚期与染色体分离时，进入成年期。这种定位与一系列有趣的生殖细胞缺陷相一致，这些缺陷是生殖细胞特征的关键决定因素。xnd-1缺失导致生殖系前体卵裂球P4在G2细胞周期停滞，从而导致动物及其后代生殖力下降，从而导致独特的“一个原始生殖细胞”表型。xnd-1突变体的不育性与转录激活相关的组蛋白修饰增加、组蛋白H3赖氨酸4（H3 K4 me 2）二甲基化以及体细胞转基因的异常表达相关，但与nos-2和nos-1的重叠作用表明转录抑制是通过多种冗余机制实现的。
The molecular pathways that govern how germ line fate is acquired is an area of intense investigation that has major implications for the development of assisted reproductive technologies, infertility interventions, and treatment of germ cell cancers. Transcriptional repression has emerged as a primary mechanism to ensure suppression of somatic growth programs in primordial germ cells. In this commentary, we address howxnd-1illuminates our understanding of transcriptional repression and how it is coordinated with the germ cell differentiation program. We recently identifiedxnd-1as a novel, early determinant of germ cell fates inCaenorhabditis elegans. Our study revealed that XND-1 is maternally deposited into early embryos where it is selectively enriched in the germ lineage and then exclusively found on chromatin in the germ lineage throughout development and into adulthood when it dissociates from chromosomes in late pachytene. This localization is consistent with a range of interesting germ cell defects that suggestxnd-1is a pivotal determinant of germ cell characteristics. Loss ofxnd-1results in a unique “one PGC (primordial germ cell)” phenotype due to G2 cell cycle arrest of the germline precursor blastomere, P4, which predisposes the animal and its progeny for reduced fecundity. The sterility inxnd-1mutants is correlated with an increase in the transcriptional activation-associated histone modification, dimethylation of histone H3 lysine 4 (H3K4me2), and aberrant expression of somatic transgenes but overlapping roles withnos-2andnos-1suggest that transcriptional repression is achieved by multiple redundant mechanisms.