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

ABSTRACT: Long non-coding RNAs (lncRNAs) are novel family of gene regulators but the study of lncRNAs in satellite cell lineage progression is still at the infancy stage. Here we identified a novel lncRNA, SAM (Sugt1 associated muscle lncRNA) that was enriched in the proliferation myoblast cells but decreased as the cells progress to differentiation. Gain- or loss- of function of SAM in muscle satellite cells altered myogenic proliferation and differentiation. The above phenotypical changes in cells were also substantiated when RNAseq was performed to assess transcriptomic changes caused by SAM loss. Gene Ontology (GO) cluster analysis of up- or down-regulated genes is in line with the pro-proliferative function of SAM and the precocious differentiation upon SAM loss.

ORGANISM(S): Mus musculus

PROVIDER: GSE126423 | GEO | 2019/11/08

REPOSITORIES: GEO

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

Project description:Long non-coding RNAs (lncRNAs) are family of gene regulators but the functional study of lncRNAs in skeletal muscle satellite cells (SCs) remains at the infancy stage. Here we identify SAM (Sugt1 associated muscle) lncRNA (also known as Snhg15, (small nucleolar RNA host gene 15) that is enriched in the proliferating myoblast cells and down-regulated as the cells progressed to differentiation. Gain- or loss- of function of SAM in muscle SCs alters myogenic proliferation and differentiation. Global deletion of SAM based on the KO-first strategy has no overt effect on mice but impairs adult muscle regeneration following acute damage; the loss also exacerbates the chronic injury induced dystrophic phenotype in the mdx mouse model. Consistently, inducible deletion of SAM in adult SCs leads to deficiency in acute injury-induced muscle regeneration. Further examination of SCs revealed that SAM loss results in cell autonomous defect in proliferative expansion of myoblasts. Mechanistically, we find SAM interacts and stabilizes Sugt1 (suppressor of G2 allele of SKP1) protein, a co-chaperon protein key to kinetochore assembly during cell division. Loss of SAM or Sugt1 both cause disruptive kinetochore assembly and microtubule attachment in mitotic cells due to mis-localization of key components Dsn1 and Hec1 proteins. Altogether, our findings identify SAM as a regulator of SC proliferation through facilitating Sugt1 mediated kinetochore assembly during cell division.

2020-05-18 | PXD018147 | Pride

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

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Suppression of Progenitor Differentiation Requires the Long Non-Coding RNA ANCR [lincRNA 391k Tiling Array V2]

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