Deletion of YY1 in satellite cells reveals its function in regulating satellite cell metabolism
Refereed conference paper presented and published in conference proceedings

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AbstractTranscription factor Yin Yang 1 (YY1) is previously known to function in regulating myoblast differentiation into myotubes but its roles during satellite cell (SC) lineage progression are unclear. Here we show that conditional deletion of YY1 in embryonic muscle progenitor cells causes severe defect of embryonic/fetal mouse muscle formation. Inducible deletion of YY1 in satellite cells (SCs) also led to striking defect in adult mouse muscle regeneration. Furthermore, YY1 deletion in dystrophic mdx mice exacerbated the dystrophic phenotype. Altogether the above data support an indispensable role of YY1 during muscle regeneration. Further analyses showed that the expansion of progenitor cells and SCs was impacted by YY1 deletion. Furthermore SCs cells from KO mice displayed cell autonomous defect in activation/proliferation as assessed by various assays. To explore the mechanisms underlying the essential role of YY1 in promoting SC activation, RNA-seq and ChIP-seq were performed. The results revealed that YY1 binds and represses a large number of mitochondrial genes in both quiescent and activating SCs, suggesting that YY1 promotes SC activation/proliferating by repressing mitochondrial respiration which may enhance glycolysis during SC activation. Our results thus identify YY1 as a key modulator of SC lineage progression through its direct regulation of stem cell metabolism.
All Author(s) ListFengyuan Chen, Jiajian Zhou, Yuying Li, Yu Zhao, Hao Sun, Huating Wang
Name of Conference8th Annual Meeting of Chinese Society for Development Biology
Start Date of Conference21/05/2017
End Date of Conference24/05/2017
Place of ConferenceNanjing
Country/Region of ConferenceChina
LanguagesEnglish-United States

Last updated on 2018-31-05 at 11:29