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TTP介导的mRNA降解对卫星细胞静止的转录后调控。

Post-transcriptional regulation of satellite cell quiescence by TTP-mediated mRNA decay.

作者信息

Hausburg Melissa A, Doles Jason D, Clement Sandra L, Cadwallader Adam B, Hall Monica N, Blackshear Perry J, Lykke-Andersen Jens, Olwin Bradley B

机构信息

Department of Molecular, Cellular, and Developmental Biology, University of Colorado Boulder, Boulder, United States.

出版信息

Elife. 2015 Mar 27;4:e03390. doi: 10.7554/eLife.03390.

DOI:10.7554/eLife.03390
PMID:25815583
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4415119/
Abstract

Skeletal muscle satellite cells in their niche are quiescent and upon muscle injury, exit quiescence, proliferate to repair muscle tissue, and self-renew to replenish the satellite cell population. To understand the mechanisms involved in maintaining satellite cell quiescence, we identified gene transcripts that were differentially expressed during satellite cell activation following muscle injury. Transcripts encoding RNA binding proteins were among the most significantly changed and included the mRNA decay factor Tristetraprolin. Tristetraprolin promotes the decay of MyoD mRNA, which encodes a transcriptional regulator of myogenic commitment, via binding to the MyoD mRNA 3' untranslated region. Upon satellite cell activation, p38α/β MAPK phosphorylates MAPKAP2 and inactivates Tristetraprolin, stabilizing MyoD mRNA. Satellite cell specific knockdown of Tristetraprolin precociously activates satellite cells in vivo, enabling MyoD accumulation, differentiation and cell fusion into myofibers. Regulation of mRNAs by Tristetraprolin appears to function as one of several critical post-transcriptional regulatory mechanisms controlling satellite cell homeostasis.

摘要

处于其微环境中的骨骼肌卫星细胞是静止的，在肌肉损伤时，它们退出静止状态，增殖以修复肌肉组织，并自我更新以补充卫星细胞群体。为了了解维持卫星细胞静止所涉及的机制，我们鉴定了在肌肉损伤后卫星细胞激活过程中差异表达的基因转录本。编码RNA结合蛋白的转录本是变化最为显著的，其中包括mRNA降解因子Tristetraprolin。Tristetraprolin通过与MyoD mRNA的3'非翻译区结合，促进编码成肌决定转录调节因子的MyoD mRNA的降解。在卫星细胞激活时，p38α/β丝裂原活化蛋白激酶（MAPK）使丝裂原活化蛋白激酶激活蛋白2（MAPKAP2）磷酸化并使Tristetraprolin失活，从而稳定MyoD mRNA。在体内对Tristetraprolin进行卫星细胞特异性敲低可过早激活卫星细胞，使MyoD积累、分化并与肌纤维融合。Tristetraprolin对mRNA的调控似乎是控制卫星细胞稳态的几种关键转录后调控机制之一。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/313f/4415119/ce55803f698d/elife03390f006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/313f/4415119/ce55803f698d/elife03390f006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/313f/4415119/8876f2f151a0/elife03390f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/313f/4415119/834f2182a58c/elife03390fs001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/313f/4415119/527cf86b0ca2/elife03390f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/313f/4415119/e0e65ae87760/elife03390fs002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/313f/4415119/e3ab093ec2c9/elife03390fs003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/313f/4415119/bcd37ba32053/elife03390f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/313f/4415119/d5fe4f49b1c9/elife03390fs004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/313f/4415119/688b88604d1f/elife03390fs005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/313f/4415119/ab499e665204/elife03390f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/313f/4415119/5d190f8f6e4a/elife03390fs006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/313f/4415119/ce55803f698d/elife03390f006.jpg

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