ArticleBiochemical and biophysical research communications2017
MPK-1/ERK regulatory network controls the number of sperm by regulating timing of sperm-oocyte switch in C. elegans germline.
Article in Biochemical and biophysical research communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Article
- Testosterone Mediates Reproductive Toxicity inToxics · 2024Article
- ADR-2 regulates fertility and oocyte fate inbioRxiv : the preprint server for biology · 2024Article
- Article
- Two distinct mechanisms lead to either oocyte or spermatocyte decrease in C. elegans after whole developmental exposure to γ-rays.PloS one · 2023Article
- Two classes of active transcription sites and their roles in developmental regulation.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Distinct roles of two eIF4E isoforms in the germline ofJournal of cell science · 2020Article
- Regulation of germ cell development by ARI1 family ubiquitin ligases in C. elegans.Scientific reports · 2018Article
- Subunits of the DNA polymerase alpha-primase complex promote Notch-mediated proliferation with discrete and shared functions in C. elegans germline.The FEBS journal · 2018Article
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Authors and funding
4 authors.
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Abstract
The precise regulation of germline sexual fate is crucial for animal fertility. In C. elegans, the production of either type of gamete, sperm or oocyte, becomes mutually exclusive beyond the larval stage. Hermaphrodites initially produce sperm and then switch to produce oocytes. This change of fate during germline development is tightly controlled by several regulators. In C. elegans hermaphrodites, FBF-1 and FBF-2 (>95% identical, members of the Pumilio RNA-binding protein family) proteins function redundantly to promote the sperm-oocyte switch. Here, we demonstrate that loss of LIP-1 (dual specificity phosphatase) in fbf-1(ok91) single mutants leads to excess sperm production due to a delayed sperm-oocyte switch. This phenotype was dramatically rescued by depletion of MPK-1 (an ERK homolog). In contrast, loss of LIP-1 in fbf-2(q738) single mutants leads to a premature sperm-oocyte switch and loss of sperm. Notably, fbf-1 fbf-2; lip-1 triple mutants produce excess sperm. These results suggest that the MPK-1/ERK regulatory network, including FBF-1, FBF-2, and LIP-1, controls the number of sperm by regulating the timing of the sperm-oocyte switch in C. elegans.
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Registered trials
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