Targeted mRNA Decay by RNA Binding Protein AUF1 Regulates Adult Muscle Stem Cell Fate, Promoting Skeletal Muscle Integrity

被引：36
|
作者：
Chenette, Devon M. [1 ]
Cadwallader, Adam B. [2 ]
Antwine, Tiffany L. [2 ]
Larkin, Lauren C. [1 ]
Wang, Jinhua [3 ]
Olwin, Bradley B. [2 ]
Schneider, Robert J. [1 ,4 ]
机构：
[1] NYU, Dept Microbiol, Sch Med, New York, NY 10016 USA
[2] Univ Colorado, Dept Mol Cellular & Dev Biol, Boulder, CO 80309 USA
[3] NYU, Ctr Hlth Informat & Bioinformat, Sch Med, New York, NY 10016 USA
[4] NYU, Perlmutter Canc Ctr, Sch Med, New York, NY 10016 USA
来源：
CELL REPORTS | 2016年 / 16卷 / 05期
关键词：
SATELLITE CELLS; MUSCULAR-DYSTROPHY; SELF-RENEWAL; MOUSE MODEL; PROGENITOR CELLS; GENE-EXPRESSION; NUCLEAR IMPORT; REGENERATION; MYOGENESIS; MAINTENANCE;
D O I：
10.1016/j.celrep.2016.06.095
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
Following skeletal muscle injury, muscle stem cells (satellite cells) are activated, proliferate, and differentiate to form myofibers. We show that mRNA-decay protein AUF1 regulates satellite cell function through targeted degradation of specific mRNAs containing 30 AU-rich elements (AREs). auf1(-/-) mice undergo accelerated skeletal muscle wasting with age and impaired skeletal muscle repair following injury. Satellite cell mRNA analysis and regeneration studies demonstrate that auf1(-/-) satellite cell self-renewal is impaired due to increased stability and overexpression of ARE-mRNAs, including cell-autonomous overexpression of matrix metalloprotease MMP9. Secreted MMP9 degrades the skeletal muscle matrix, preventing satellite-cell-mediated regeneration and return to quiescence. Blocking MMP9 activity in auf1(-/-) mice restores skeletal muscle repair and maintenance of the satellite cell population. Control of ARE-mRNA decay by AUF1 represents a mechanism for adult stem cell regulation and is implicated in human skeletal muscle wasting diseases.
引用
收藏
页码：1379 / 1390
页数：12
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