期刊
DEVELOPMENTAL CELL
卷 34, 期 1, 页码 96-107出版社
CELL PRESS
DOI: 10.1016/j.devcel.2015.05.014
关键词
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资金
- National Institute of Genetics (NIG)
- Japan Society for the Promotion of Science (KAKENHI) [21227008, 26251025]
- Ministry of Education, Culture, Sports, Science, and Technology of Japan t [25112002]
- Transdisciplinary Research Integration Center of the Research Organization of Information and Systems
- Grants-in-Aid for Scientific Research [25112002, 25114004] Funding Source: KAKEN
In many adult tissues, homeostasis relies on self-renewing stem cells that are primed for differentiation. The reconciliation mechanisms of these characteristics remain a fundamental question in stem cell biology. We propose that regulation at the post-transcriptional level is essential for homeostasis in murine spermatogonial stem cells (SSCs). Here, we show that Nanos2, an evolutionarily conserved RNA-binding protein, works with other cellular messenger ribonucleoprotein (mRNP) components to ensure the primitive status of SSCs through a dual mechanism that involves (1) direct recruitment and translational repression of genes that promote spermatogonial differentiation and (2) repression of the target of rapamycin complex 1 (mTORC1), a well-known negative pathway for SSC self-renewal, by sequestration of the core factor mTOR in mRNPs. This mechanism links mRNA turnover to mTORC1 signaling through Nanos2-containing mRNPs and establishes a post-transcriptional buffering system to facilitate SSC homeostasis in the fluctuating environment within the seminiferous tubule.
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