The Two‐pore channel 2 (TPC2) mediates autophagy in skeletal muscles

Abstract

Nicotinic acid adenine dinucleotide phosphate (NAADP) is a potent Ca2+‐mobilizing messenger that in many cells releases Ca2+ from the endolysosomal system. Recent studies have shown that NAADP‐induced Ca2+ mobilization is mediated by the two‐pore channels (TPCs). The objective of this study is to test whether TPC2 is involved in autophagy in skeletal muscle.MethodsWild type or TPC2 null animals were subjected to autophagy induction to compare the autophagy fluxes in the animals. In some experiments, isolated neonatal myoblasts were used. Detection methods include LC3 western blot and electron micrographs.Summary of results and conclusions: Our data provide evidence that TPC2 is involved in regulating autophagy flux in skeletal muscle. TPC2 mutant demonstrated defective autophagy to maintain tissue homeostasis.Summary of funding: There is no NIH funding to support this research project yet.