ArticlePLoS genetics2020
PCH-2 collaborates with CMT-1 to proofread meiotic homolog interactions.
Article in PLoS genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Oocyte-specific acylglycerol kinase loss leads to infertility in mice via mitochondrial dysfunction.Communications biology · 2026Article
- Exportin-mediated nucleocytoplasmic transport maintains Pch2 homeostasis during meiosis.PLoS genetics · 2023Article
- The conserved AAA ATPase PCH-2 distributes its regulation of meiotic prophase events through multiple meiotic HORMADs in C. elegans.PLoS genetics · 2023Article
- PCH-2 and meiotic HORMADs: A module for evolutionary innovation in meiosis?Current topics in developmental biology · 2023Review
- ZYP1-mediated recruitment of PCH2 to the synaptonemal complex remodels the chromosome axis leading to crossover restriction.Nucleic acids research · 2022Article
- Review
- Aberrant Expression of Mitochondrial SAM Transporter SLC25A26 Impairs Oocyte Maturation and Early Development in Mice.Oxidative medicine and cellular longevity · 2022Article
- Mad1's ability to interact with Mad2 is essential to regulate and monitor meiotic synapsis in C. elegans.PLoS genetics · 2021Article
- Getting there: understanding the chromosomal recruitment of the AAA+ ATPase Pch2/TRIP13 during meiosis.Current genetics · 2021Review
- Pch2 orchestrates the meiotic recombination checkpoint from the cytoplasm.PLoS genetics · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The conserved ATPase, PCH-2/TRIP13, is required during both the spindle checkpoint and meiotic prophase. However, its specific role in regulating meiotic homolog pairing, synapsis and recombination has been enigmatic. Here, we report that this enzyme is required to proofread meiotic homolog interactions. We generated a mutant version of PCH-2 in C. elegans that binds ATP but cannot hydrolyze it: pch-2E253Q. In vitro, this mutant can bind a known substrate but is unable to remodel it. This mutation results in some non-homologous synapsis and impaired crossover assurance. Surprisingly, worms with a null mutation in PCH-2's adapter protein, CMT-1, the ortholog of p31comet, localize PCH-2 to meiotic chromosomes, exhibit non-homologous synapsis and lose crossover assurance. The similarity in phenotypes between cmt-1 and pch-2E253Q mutants suggest that PCH-2 can bind its meiotic substrates in the absence of CMT-1, in contrast to its role during the spindle checkpoint, but requires its adapter to hydrolyze ATP and remodel them.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.