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DAF-18/PTEN 在原始生殖细胞静止期间抑制生殖细胞-合子基因的激活。

DAF-18/PTEN inhibits germline zygotic gene activation during primordial germ cell quiescence.

机构信息

Skirball Institute of Biomolecular Medicine, Department of Cell Biology, NYU Grossman School of Medicine, New York, New York, United States of America.

Department of Biology, Center for Genomic and Computational Biology, Duke University, Durham, North Carolina, United States of America.

出版信息

PLoS Genet. 2021 Jul 21;17(7):e1009650. doi: 10.1371/journal.pgen.1009650. eCollection 2021 Jul.

DOI:10.1371/journal.pgen.1009650
PMID:34288923
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8294487/
Abstract

Quiescence, an actively-maintained reversible state of cell cycle arrest, is not well understood. PTEN is one of the most frequently lost tumor suppressors in human cancers and regulates quiescence of stem cells and cancer cells. The sole PTEN ortholog in Caenorhabditis elegans is daf-18. In a C. elegans loss-of-function mutant for daf-18, primordial germ cells (PGCs) divide inappropriately in L1 larvae hatched into starvation conditions, in a TOR-dependent manner. Here, we further investigated the role of daf-18 in maintaining PGC quiescence in L1 starvation. We found that maternal or zygotic daf-18 is sufficient to maintain cell cycle quiescence, that daf-18 acts in the germ line and soma, and that daf-18 affects timing of PGC divisions in fed animals. Importantly, our results also implicate daf-18 in repression of germline zygotic gene activation, though not in germline fate specification. However, TOR is less important to germline zygotic gene expression, suggesting that in the absence of food, daf-18/PTEN prevents inappropriate germline zygotic gene activation and cell division by distinct mechanisms.

摘要

静止状态，一种主动维持的细胞周期阻滞可逆状态，目前还了解得不够透彻。PTEN 是人类癌症中最常丢失的肿瘤抑制因子之一，可调节干细胞和癌细胞的静止状态。秀丽隐杆线虫中唯一的 PTEN 直系同源物是 daf-18。在 daf-18 的秀丽隐杆线虫功能丧失突变体中，原始生殖细胞（PGCs）在 L1 幼虫孵化到饥饿条件下时会以 TOR 依赖性的方式不恰当地分裂。在这里，我们进一步研究了 daf-18 在维持 L1 饥饿状态下 PGC 静止状态中的作用。我们发现母体或合子 daf-18 足以维持细胞周期静止状态，daf-18 在生殖系和体躯中起作用，并且 daf-18 影响喂食动物中 PGC 分裂的时间。重要的是，我们的结果还表明 daf-18 参与抑制生殖系合子基因激活，但不参与生殖系命运特化。然而，TOR 对生殖系合子基因表达的重要性较低，这表明在没有食物的情况下，daf-18/PTEN 通过不同的机制防止不适当的生殖系合子基因激活和细胞分裂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0920/8294487/33db4dddf62a/pgen.1009650.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0920/8294487/483537abf603/pgen.1009650.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0920/8294487/f2a9de7d98d3/pgen.1009650.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0920/8294487/e62129cf2b73/pgen.1009650.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0920/8294487/4d09b2a8a3cb/pgen.1009650.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0920/8294487/2446e020cab7/pgen.1009650.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0920/8294487/1d28fe1d2c3a/pgen.1009650.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0920/8294487/33db4dddf62a/pgen.1009650.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0920/8294487/483537abf603/pgen.1009650.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0920/8294487/f2a9de7d98d3/pgen.1009650.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0920/8294487/e62129cf2b73/pgen.1009650.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0920/8294487/4d09b2a8a3cb/pgen.1009650.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0920/8294487/2446e020cab7/pgen.1009650.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0920/8294487/1d28fe1d2c3a/pgen.1009650.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0920/8294487/33db4dddf62a/pgen.1009650.g007.jpg

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