Voltage- induced calcium release in Caenorhabditis elegans body muscles

• 成果类型: Article
• 署名作者: Gao, Luna; Ardiel, Evan; Nurrish, Stephen; Kaplan, Joshua M.
• 署名单位: Harvard University; Harvard University Medical Affiliates; Massachusetts General Hospital; Harvard University; Harvard Medical School; Harvard University; Harvard Medical School
• 刊物名称: PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
• ISSN/ISSBN: 0027-12367
• DOI: 10.1073/pnas.2317753121
• 发表日期: 2024-05-07
• 关键词: resting energy-expenditure; dihydropyridine receptors; ryanodine receptor; surface-temperature; oral-contraceptives; channel activity; menstrual-cycle; ca2+ release; cold; contraction

摘要

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.