AI Article Synopsis
- * In C. elegans, the gene mctp-1 is regulated by two promoters: one in the nervous system and another in the spermatheca.
- * Loss of mctp-1 function leads to egg-laying issues and reduced movement, and mutants show decreased sensitivity to the drug aldicarb, indicating that MCTP-1 may influence synaptic vesicle release.
Article Abstract
Multiple C2 and Transmembrane Domain Proteins (MCTPs) are putative calcium sensors. Proteins that contain C2 domains play essential roles in membrane trafficking and exocytosis; however, MCTPs functions in neurotransmitter release are not known. Here we report that in C. elegans mctp-1 is under the control of two promoters - one active in the nervous system and the second in the spermatheca. We generated and characterized a loss of function amt1 mutant and compared it to a previously published loss of function mutant (av112). Loss of mctp-1 function causes defects in egg-laying, crawling velocity, and thrashing rates. Both amt1 and av112 mutants are hyposensitive to the acetylcholinesterase blocker aldicarb, suggesting that MCTP-1 may play a role in synaptic vesicle release.
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| http://dx.doi.org/10.1016/j.mcn.2020.103528 | DOI Listing |
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