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om92 , a glp-1 enhancer mutation, is an allele of ekl-1
Germline stem cell proliferation in C. elegans requires activation of the GLP-1/Notch receptor, which is located on the germline plasma membrane and encoded by the glp-1 gene. We previously identified several genes whose products directly or indirectly promote activity of the GLP-1 signaling pathway...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Caltech Library
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9756089/ https://www.ncbi.nlm.nih.gov/pubmed/36530475 http://dx.doi.org/10.17912/micropub.biology.000698 |
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author | Stein, Samantha A. Zucaro, Olivia F. Smith, Harold E. O'Connell, Kevin F. Spoerke, Jill M. Maine, Eleanor M. Lissemore, James L. |
author_facet | Stein, Samantha A. Zucaro, Olivia F. Smith, Harold E. O'Connell, Kevin F. Spoerke, Jill M. Maine, Eleanor M. Lissemore, James L. |
author_sort | Stein, Samantha A. |
collection | PubMed |
description | Germline stem cell proliferation in C. elegans requires activation of the GLP-1/Notch receptor, which is located on the germline plasma membrane and encoded by the glp-1 gene. We previously identified several genes whose products directly or indirectly promote activity of the GLP-1 signaling pathway by finding mutations that enhance the germline phenotype of a glp-1(ts) allele, glp-1(bn18) . Here, we report phenotypic and molecular analysis of a new ekl-1 allele, ekl-1(om92) , that enhances the glp-1(bn18) phenotype. ekl-1(om92) is a 244 bp deletion predicted to generate a frameshift and premature termination codon, yielding a severely truncated protein, suggesting it is a null allele. |
format | Online Article Text |
id | pubmed-9756089 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Caltech Library |
record_format | MEDLINE/PubMed |
spelling | pubmed-97560892022-12-17 om92 , a glp-1 enhancer mutation, is an allele of ekl-1 Stein, Samantha A. Zucaro, Olivia F. Smith, Harold E. O'Connell, Kevin F. Spoerke, Jill M. Maine, Eleanor M. Lissemore, James L. MicroPubl Biol New Finding Germline stem cell proliferation in C. elegans requires activation of the GLP-1/Notch receptor, which is located on the germline plasma membrane and encoded by the glp-1 gene. We previously identified several genes whose products directly or indirectly promote activity of the GLP-1 signaling pathway by finding mutations that enhance the germline phenotype of a glp-1(ts) allele, glp-1(bn18) . Here, we report phenotypic and molecular analysis of a new ekl-1 allele, ekl-1(om92) , that enhances the glp-1(bn18) phenotype. ekl-1(om92) is a 244 bp deletion predicted to generate a frameshift and premature termination codon, yielding a severely truncated protein, suggesting it is a null allele. Caltech Library 2022-11-30 /pmc/articles/PMC9756089/ /pubmed/36530475 http://dx.doi.org/10.17912/micropub.biology.000698 Text en Copyright: © 2022 by the authors https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | New Finding Stein, Samantha A. Zucaro, Olivia F. Smith, Harold E. O'Connell, Kevin F. Spoerke, Jill M. Maine, Eleanor M. Lissemore, James L. om92 , a glp-1 enhancer mutation, is an allele of ekl-1 |
title |
om92
, a
glp-1
enhancer mutation, is an allele of
ekl-1
|
title_full |
om92
, a
glp-1
enhancer mutation, is an allele of
ekl-1
|
title_fullStr |
om92
, a
glp-1
enhancer mutation, is an allele of
ekl-1
|
title_full_unstemmed |
om92
, a
glp-1
enhancer mutation, is an allele of
ekl-1
|
title_short |
om92
, a
glp-1
enhancer mutation, is an allele of
ekl-1
|
title_sort | om92
, a
glp-1
enhancer mutation, is an allele of
ekl-1 |
topic | New Finding |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9756089/ https://www.ncbi.nlm.nih.gov/pubmed/36530475 http://dx.doi.org/10.17912/micropub.biology.000698 |
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