ArticleG3 (Bethesda, Md.)2022
A sensitized genetic screen to identify regulators of Caenorhabditis elegans germline stem cells.
Article in G3 (Bethesda, Md.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Review
- Analysis of Notch1 signaling in mammalian sperm development.BMC research notes · 2023Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
GLP-1/Notch signaling and a downstream RNA regulatory network maintain germline stem cells in Caenorhabditis elegans. In mutants lacking the GLP-1 receptor, all germline stem cells enter the meiotic cell cycle precociously and differentiate into sperm. This dramatic germline stem cell defect is called the "Glp" phenotype. The lst-1 and sygl-1 genes are direct targets of Notch transcriptional activation and functionally redundant. Whereas single lst-1 and sygl-1 mutants are fertile, lst-1 sygl-1 double mutants are sterile with a Glp phenotype. We set out to identify genes that function redundantly with either lst-1 or sygl-1 to maintain germline stem cells. To this end, we conducted forward genetic screens for mutants with a Glp phenotype in genetic backgrounds lacking functional copies of either lst-1 or sygl-1. The screens generated 9 glp-1 alleles, 2 lst-1 alleles, and 1 allele of pole-1, which encodes the catalytic subunit of DNA polymerase ε. Three glp-1 alleles reside in Ankyrin repeats not previously mutated. pole-1 single mutants have a low penetrance Glp phenotype that is enhanced by loss of sygl-1. Thus, the screen uncovered 1 locus that interacts genetically with sygl-1 and generated useful mutations for further studies of germline stem cell regulation.
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Registered trials
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