Long noncoding RNA SAM promotes myoblast proliferation through stabilizing Sugt1 and facilitating kinetochore assembly
Yuying Li,
Jie Yuan,
Fengyuan Chen,
Suyang Zhang,
Yu Zhao,
Xiaona Chen,
Leina Lu,
Liang Zhou,
Ching Yan Chu,
Hao Sun () and
Huating Wang ()
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Yuying Li: The Chinese University of Hong Kong
Jie Yuan: The Chinese University of Hong Kong
Fengyuan Chen: The Chinese University of Hong Kong
Suyang Zhang: The Chinese University of Hong Kong
Yu Zhao: The Chinese University of Hong Kong
Xiaona Chen: The Chinese University of Hong Kong
Leina Lu: The Chinese University of Hong Kong
Liang Zhou: Southern Medical University
Ching Yan Chu: The Chinese University of Hong Kong
Hao Sun: The Chinese University of Hong Kong
Huating Wang: The Chinese University of Hong Kong
Nature Communications, 2020, vol. 11, issue 1, 1-16
Abstract:
Abstract The functional study of lncRNAs in skeletal muscle satellite cells (SCs) remains at the infancy stage. Here we identify SAM (Sugt1 asssociated muscle) lncRNA that is enriched in the proliferating myoblasts. Global deletion of SAM has no overt effect on mice but impairs adult muscle regeneration following acute damage; it also exacerbates the chronic injury-induced dystrophic phenotype in mdx mice. Consistently, inducible deletion of SAM in SCs leads to deficiency in muscle regeneration. Further examination reveals that SAM loss results in a cell-autonomous defect in the proliferative expansion of myoblasts. Mechanistically, we find SAM interacts and stabilizes Sugt1, a co-chaperon protein key to kinetochore assembly during cell division. Loss of SAM or Sugt1 both disrupts kinetochore assembly in mitotic cells due to the mislocalization of two components: Dsn1 and Hec1. Altogether, our findings identify SAM as a regulator of SC proliferation through facilitating Sugt1 mediated kinetochore assembly during cell division.
Date: 2020
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DOI: 10.1038/s41467-020-16553-6
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