Abstract
Stac3 regulates excitation-contraction coupling (EC coupling) in vertebrate skeletal muscles by regulating the L-type voltage-gated calcium channel (Cav channel). Recently a stac-like gene, Dstac, was identified in Drosophila and found to be expressed by both a subset of neurons and muscles. Here, we show that Dstac and Dmca1D, the Drosophila L-type Cav channel, are necessary for normal locomotion by larvae. Immunolabeling with specific antibodies against Dstac and Dmca1D found that Dstac and Dmca1D are expressed by larval body-wall muscles. Furthermore, Ca2+ imaging of muscles of Dstac and Dmca1D deficient larvae found that Dstac and Dmca1D are required for excitation-contraction coupling. Finally, Dstac appears to be required for normal expression levels of Dmca1D in body-wall muscles. These results suggest that Dstac regulates Dmca1D during EC coupling and thus muscle contraction.
Highlights
Muscle contractions are initiated by depolarizations of muscle membrane potential due to the release of neurotransmitter at the neuromuscular junction
We found that Drosophila larvae in which Dmca1D was selectively knocked down in body wall muscles exhibited decreased muscle Ca2+ transients and locomotion
Our results are consistent with the possibility that Ca2+ influx via Dmca1D might initiate Ca2+ induced Ca2+ release (CICR) that leads to Ca2+ transients during EC coupling and muscle contraction
Summary
Muscle contractions are initiated by depolarizations of muscle membrane potential due to the release of neurotransmitter at the neuromuscular junction. EC coupling is the process that transduces changes in membrane voltage to increases in cytosolic Ca2+ due to the release of Ca2+ from the sarcoplasmic reticulum (SR) and subsequently contraction. Stac regulates EC coupling in murine skeletal muscles (Nelson et al, 2013) and murine muscle development (Ge et al, 2014; Cong et al, 2016). In zebrafish skeletal muscles Stac colocalizes with DHPR and RyR and regulates DHPR levels, stability and functionality, including the voltage response of DHPRs but not trafficking of DHPRs (Linsley et al, 2017a,b). Stac appears not to be required for normal levels or functionality of RyRs,
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