2. Academic Validation
  3. Long noncoding RNA SAM promotes myoblast proliferation through stabilizing Sugt1 and facilitating kinetochore assembly

Long noncoding RNA SAM promotes myoblast proliferation through stabilizing Sugt1 and facilitating kinetochore assembly

  • Nat Commun. 2020 Jun 1;11(1):2725. doi: 10.1038/s41467-020-16553-6.
Yuying Li 1,  Jie Yuan 1,  Fengyuan Chen 2,  Suyang Zhang 2,  Yu Zhao 2,  Xiaona Chen 2,  Leina Lu 1 3 4,  Liang Zhou 5,  Ching Yan Chu 6,  Hao Sun 7 8,  Huating Wang 9 10
Affiliations

Affiliations

  • 1 Department of Chemical Pathology, The Chinese University of Hong Kong, Hong Kong, China.
  • 2 Department of Orthaepedics and Traumatology, The Chinese University of Hong Kong, Hong Kong, China.
  • 3 Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong, China.
  • 4 Department of Genetics and Genome Sciences, School of Medicine, Case Western Reserve University, Cleveland, 44106, OH, USA.
  • 5 Department of Toxicology, School of Public Health, Southern Medical University, Guangzhou, China.
  • 6 Department of Obstetrics and Gynaecology, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong, China.
  • 7 Department of Chemical Pathology, The Chinese University of Hong Kong, Hong Kong, China. haosun@cuhk.edu.hk.
  • 8 Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong, China. haosun@cuhk.edu.hk.
  • 9 Department of Orthaepedics and Traumatology, The Chinese University of Hong Kong, Hong Kong, China. huating.wang@cuhk.edu.hk.
  • 10 Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong, China. huating.wang@cuhk.edu.hk.
PMID: 32483152 DOI: 10.1038/s41467-020-16553-6
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.

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