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Peer-reviewedCC BYmicroPublication Biology

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

  • James L. Lissemore1
  • Amanda Pancake1
  • Shurong Fang2
  • Eleanor M. Maine3
  1. 1Department of Biology, John Carroll University, University Heights, OH, USA
  2. 2Department of Mathematics, Computer Science, and Data Science, John Carroll University, University Heights, OH, USA
  3. 3Department of Biology, Syracuse University, Syracuse, NY, USA
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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.

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Cite

BibTeXRIS
BibTeX
@article{lissemore2026elegans,
  title = {{The C. elegans endoplasmic reticulum molecular chaperone ENPL-1 does not promote GLP-1/Notch signaling}},
  author = {James L. Lissemore and Amanda Pancake and Shurong Fang and Eleanor M. Maine},
  journal = {microPublication Biology},
  year = {2026},
  month = jul,
  doi = {10.17912/micropub.biology.002171},
  url = {https://doi.org/10.17912/micropub.biology.002171},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - The C. elegans endoplasmic reticulum molecular chaperone ENPL-1 does not promote GLP-1/Notch signaling
AU  - James L. Lissemore
AU  - Amanda Pancake
AU  - Shurong Fang
AU  - Eleanor M. Maine
PY  - 2026
DA  - 2026/07/01
JO  - microPublication Biology
DO  - 10.17912/micropub.biology.002171
UR  - https://doi.org/10.17912/micropub.biology.002171
AB  - 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.
SN  - 2578-9430
ER  -