Expression and function of Caenorhabditis elegans UNCP-18, a paralog of the SM protein UNC-18.
| Autor: | Boeglin M; Department of Biological Sciences, Columbia University, Howard Hughes Medical Institute, NewYork, NY 10027, USA.; Department of Development and Stem Cells, IGBMC, CNRS UMR 7104/INSERM U1258, Université de Strasbourg, Strasbourg 67081, France., Leyva-Díaz E; Department of Biological Sciences, Columbia University, Howard Hughes Medical Institute, NewYork, NY 10027, USA., Hobert O; Department of Biological Sciences, Columbia University, Howard Hughes Medical Institute, NewYork, NY 10027, USA. |
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| Jazyk: | angličtina |
| Zdroj: | Genetics [Genetics] 2023 Dec 06; Vol. 225 (4). |
| DOI: | 10.1093/genetics/iyad180 |
| Abstrakt: | Sec1/Munc18 (SM) proteins are important regulators of SNARE complex assembly during exocytosis throughout all major animal tissue types. However, expression of a founding member of the SM family, UNC-18, is mostly restricted to the nervous system of the nematode Caenorhabditis elegans, where it is important for synaptic transmission. Moreover, unc-18 null mutants do not display the lethality phenotype associated with (a) loss of all Drosophila and mouse orthologs of unc-18 and (b) with complete elimination of synaptic transmission in C. elegans. We investigated whether a previously uncharacterized unc-18 paralog, which we named uncp-18, may be able to explain the restricted expression and limited phenotypes of unc-18 null mutants. A reporter allele shows ubiquitous expression of uncp-18. Analysis of uncp-18 null mutants, unc-18 and uncp-18 double null mutants, as well as overexpression of uncp-18 in an unc-18 null mutant background, shows that these 2 genes can functionally compensate for one another and are redundantly required for embryonic viability. Our results indicate that the synaptic transmission defects of unc-18 null mutants cannot necessarily be interpreted as constituting a null phenotype for SM protein function at the synapse. Competing Interests: Conflicts of interest The authors declare no conflict of interest. (© The Author(s) 2023. Published by Oxford University Press on behalf of The Genetics Society of America.) |
| Databáze: | MEDLINE |
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