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:We created mice, which are deficient for Myc specifically in cardiac myocytes by crossing crossed Myc-floxed mice (Mycfl/fl) and MLC-2VCre/+ mice. Serial analysis of earlier stages of gestation revealed that Myc-deficient mice died prematurely at E13.5-14.5. Morphological analyses of E13.5 Myc-null embryos showed normal ventricular size and structure; however, decreased cardiac myocyte proliferation and increased apoptosis was observed. BrdU incorporation rates were also decreased significantly in Myc-null myocardium. Myc-null mice displayed a 3.67-fold increase in apoptotic cardiomyocytes by TUNEL assay. We examined global gene expression using oligonucleotide microarrays. Numerous genes involved in mitochondrial death pathways were dysregulated including Bnip3L and Birc2. Keywords: wildtype vs Myc-null
