The C. elegans endoplasmic reticulum molecular chaperone ENPL-1 does not promote GLP-1/Notch signaling.

Authors

James L Lissemore, Amanda Pancake, Shurong Fang, Eleanor M Maine

Published in

microPublication biology. Volume 2026. Epub Jul 08, 2026.

Abstract

The C. elegans Notch receptor, GLP-1 , is essential for germline proliferation and early embryonic development. While the cytosolic chaperone HSP-90 promotes GLP-1 signaling in the germline, it is unknown whether the endoplasmic reticulum-resident Hsp90, ENPL-1 (GRP94/endoplasmin), also promotes GLP-1 signaling. We used RNAi knockdown of enpl-1 in a sensitized glp-1 ( bn18 ) background to investigate potential genetic interactions. RNAi-mediated knockdown of enpl-1 did not enhance reduced GLP-1 /Notch signaling, and it caused a similar degree of early larval arrest in both wildtype and glp-1 ( bn18 ) backgrounds. Thus, we did not detect a role for ENPL-1 in promoting GLP-1 /Notch signaling.

PMID:
42502752
Bibliographic data and abstract were imported from PubMed on 26 Jul 2026.

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