Frieden group publishes a study defining mechanisms of fast Ca2+ signalling in human muscle cells
The group of Dr. Maud Frieden recently published a report in Biochemica et Biophysica Acta – Molecular Cell Research entitled “TRPC1 and TRPC4 channels functionally interact with STIM1L to promote myogenesis and maintain fast repetitive Ca2+ release in human myotubes”. In this study, led by former post-doc Fabrice Antigny, now a researcher at the French Institute of Health and Medical Research at the INSERM, Paris, the authors further define the molecular players of a process called store-operated Ca2+ entry in a cellular model of human muscle.
The classic model of muscle contraction involves the release of Ca2+ from intracellular stores, called the sarcoplasmic reticulum (SR), in response to voltage changes on the muscle membrane caused by signals coming from the nervous system. Yet the SR is a finite Ca2+ store that needs to be refilled in order to sustain multiple rounds of signalling. The recent discovery of a muscle-specific isoform of a gene that is important for the refilling of the SR called STIM1L, by the group of Prof. Laurent Bernheim in collaboration with the Frieden group, has led to a significant advancement of our understanding of Ca2+ signals during muscle regeneration. In the present study, Fabrice and colleagues further characterize the mechanisms by which STIM1L operates by identifying two Ca2+ channels TRPC1 and TRPC4 as functional partners of STIM1L in human myotubes. They not only show that functional coupling between these two channels with STIM1L is required for sustained fast Ca2+ signals, but that these three genes are important for muscle development and regeneration as well.
Posted by: P. Nunes-HaslerApril 19, 2017