Project description:To get insight into the transcriptomic changes caused by HDAC11 loss at early myogenic differentiation, we performed RNA sequencing (RNA-Seq) in 24 h differentiated primary myoblasts from WT and HDAC11-deficient mice. Satellite cell-derived primary myoblasts were obtained after FACS isolation of skeletal muscle cells by growing them at low confluence in proliferation medium. To induce myoblast differentiation, cells were plated at high confluence and changed to differentiation media. Gene Ontology (GO) analysis of the genes upregulated in HDAC11 KO differentiating myoblasts revealed a statistically significant enrichment of cell cycle-related processes while the downregulated genes in HDAC11 KO differentiating myoblasts were enriched in “muscle system process” and “muscle contraction” GO categories.
Project description:Knockdown of PRDM2 led to precocious differentiation. To understand the molecular basis for this phenotype, we performed microaary analysis of 28hr differentiated myoblasts. Genes differentially regulated by PRDM2 knock down were reveraled by microarray analysis using affymetrix mouse chips.
Project description:Adult skeletal muscle is a plastic tissue that can adapt its size to workload and that can regenerate after demage. Here, we show that RhoA within primary myoblasts is needed for a correct muscle regeneration by controlling satellite cell fusion without affecting their proliferation or their differentiation. Moreover primary cultured myoblast loosing RhoA have no defects in cytoskeleton reorganization however their movement is altered compared to control cells. At the molecular level, we found that RhoA controls the expressions of different genes depending on step of differentiation process, not necessarly already described as implicated in fusion program. These findings unravel the implication of RhoA within satellite cells regulating myoblast fusion in response to demage in order to allow a correct regeneration process.
Project description:Maps of genomic regions in proximity to the nuclear lamina were determined in undifferentiated C2C12 myoblasts (MBs) and 6 day differentiated C2C12 myotubes (MTs) using DamID with a Dam-Lamin B1-encoding lentivirus.