Voltage-induced calcium release in Caenorhabditis elegans body muscles

Author:

Gao Luna12,Ardiel Evan12,Nurrish Stephen12ORCID,Kaplan Joshua M.123ORCID

Affiliation:

1. Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114

2. Department of Neurobiology, Harvard Medical School, Boston, MA 02115

3. Program in Neuroscience, Harvard Medical School, Boston, MA 02115

Abstract

Type 1 voltage-activated calcium channels (CaV1) in the plasma membrane trigger calcium release from the sarcoplasmic reticulum (SR) by two mechanisms. In voltage-induced calcium release (VICR), CaV1 voltage sensing domains are directly coupled to ryanodine receptors (RYRs), an SR calcium channel. In calcium-induced calcium release (CICR), calcium ions flowing through activated CaV1 channels bind and activate RYR channels. VICR is thought to occur exclusively in vertebrate skeletal muscle while CICR occurs in all other muscles (including all invertebrate muscles). Here, we use calcium-activated SLO-2 potassium channels to analyze CaV1-SR coupling in Caenorhabditis elegans body muscles. SLO-2 channels were activated by both VICR and external calcium. VICR-mediated SLO-2 activation requires two SR calcium channels (RYRs and IP3 Receptors), JPH-1/Junctophilin, a PDZ (PSD95, Dlg1, ZO-1 domain) binding domain (PBD) at EGL-19/CaV1’s carboxy-terminus, and SHN-1/Shank (a scaffolding protein that binds EGL-19’s PBD). Thus, VICR occurs in invertebrate muscles.

Funder

HHS | National Institutes of Health

Publisher

Proceedings of the National Academy of Sciences

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