Gastrocnemius muscle-Deletion of TECRL promotes skeletal muscle repair
Myogenic regeneration relies on the proliferation and differentiation of satellite cells. TECRL (Trans-2,3-Enoyl-CoA Reductase Like) is an endoplasmic reticulum protein only expressed in cardiac and skeletal muscle. However, its role in myogenesis remains unknown. We show that TECRL expression is increased in response to ischemic injury. Satellite cell-specific deletion of TECRL enhances muscle repair by increasing the expression of EGR2 through the activation of the ERK1/2 signaling pathway, which in turn promotes the expression of PAX7. We further showed that TECRL deletion led to the upregulation of the histone acetyltransferase general control non-derepressible 5 (GCN5), which enhances the transcription of EGR2 through acetylation. Overall design: Total RNA from TECRLflox/flox and TECRLscko gastrocnemius muscle.  TECRLscko mice (satellite cell – specific TECRL knockout mice) were generated by crossing Pax7-Cre mice (Stock Number: 010530, Pax7tm1 (cre) Mrc/J; The Jackson Laboratory, Bar Harbor, ME) with TECRLflox/flox mice (generated by Cyagen, Guangzhou, China).