Distinct transcriptomic changes in E14.5 mouse skeletal muscle lacking RYR1 or Cav1.1 converge at E18.5

摘要: In skeletal muscle the coordinated actions of two mechanically coupled Ca2+ channels-the 1,4-dihydropyridine receptor (Cav1.1) and type 1 ryanodine (RYR1)-underlie molecular mechanism rapid cytosolic [Ca2+] increase leading to contraction. While both [Ca2+]i contractile activity have been implicated in regulation myogenesis, less is known about potential specific roles Cav1.1 RYR1 development. this study, we analyzed histology transcriptomic changes occurring at E14.5 -the end primary myogenesis around onset intrauterine limb movement, E18.5 secondary WT, RYR1-/-, Cav1.1-/- murine muscle. At mutants exhibited initial alterations, which became much more severe E18.5. Immunohistological analysis also revealed higher levels activated caspase-3 muscles E14.5, indicating an apoptosis. With WT littermates as controls, microarray analyses identified 61 97 differentially regulated genes (DEGs) 493 1047 DEGs E18.5, RYR1-/- samples, respectively. Gene enrichment detected no overlap affected biological processes pathways whereas there was a significant mutants, affecting predominantly linked Moreover, vs. comparison multiple genotype-specific involved contraction, cell cycle miRNA-mediated signaling neuronal bone development lipid metabolism samples. Taken together, our study reveals discrete global transcriptome from mice. Our results suggest distinct functional for myogenesis.