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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...

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Detalles Bibliográficos
Autores principales: Stein, Samantha A., Zucaro, Olivia F., Smith, Harold E., O'Connell, Kevin F., Spoerke, Jill M., Maine, Eleanor M., Lissemore, James L.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Caltech Library 2022
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
Descripción
Sumario: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.