ArticleGenetics2009
Drosophila PCH2 is required for a pachytene checkpoint that monitors double-strand-break-independent events leading to meiotic crossover formation.
Article in Genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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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.
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Who cites it
62 citing papers in PubMed, 101 citations in OpenAlex.
- Meiotic pairing through barcode-like satellite DNA repeats.Nature communications · 2026Article
- Programmed meiotic errors facilitate dichotomous sperm production in the silkworm,Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- The Drosophila mauritiana synaptonemal complex protein C(3)G repatterns the recombination landscape of Drosophila melanogaster.PLoS genetics · 2025Article
- Distinct cellular and reproductive consequences of meiotic chromosome synapsis defects in syce2 and sycp1 mutant zebrafish.PLoS genetics · 2025Article
- Thyroid hormone receptor interacting protein 13 is associated with prognosis and immunotherapy efficacy in human cancers: a pan-cancer analysis.Discover oncology · 2025Article
- Article
- The conserved ATPase PCH-2 controls the number and distribution of crossovers by antagonizing their formation inbioRxiv : the preprint server for biology · 2024Article
- Role of TRIP13 in human cancer development.Molecular biology reports · 2024Review
- Analysis of meiotic recombination in Drosophila simulans shows no evidence of an interchromosomal effect.Genetics · 2024Article
- TI17, a novel compound, exerts anti-MM activity by impairing Trip13 function of DSBs repair and enhancing DNA damage.Cancer medicine · 2023Article
- Targeting TRIP13 for overcoming anticancer drug resistance (Review).Oncology reports · 2023Article
- Exportin-mediated nucleocytoplasmic transport maintains Pch2 homeostasis during meiosis.PLoS genetics · 2023Article
- TRIP 13-dependent pathways promote the development of gastric cancer.Functional & integrative genomics · 2023Article
- PCH-2 and meiotic HORMADs: A module for evolutionary innovation in meiosis?Current topics in developmental biology · 2023Review
- A Brief History ofGenes · 2022Review
- Article
- Does the Pachytene Checkpoint, a Feature of Meiosis, Filter Out Mistakes in Double-Strand DNA Break Repair and as a side-Effect Strongly Promote Adaptive Speciation?Integrative organismal biology (Oxford, England) · 2022Article
- OsPRD2 is essential for double-strand break formation, but not spindle assembly during rice meiosis.Frontiers in plant science · 2022Article
- Article
- Meiosis in crops: from genes to genomes.Journal of experimental botany · 2021Review
2 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During meiosis, programmed DNA double-strand breaks (DSBs) are repaired to create at least one crossover per chromosome arm. Crossovers mature into chiasmata, which hold and orient the homologous chromosomes on the meiotic spindle to ensure proper segregation at meiosis I. This process is usually monitored by one or more checkpoints that ensure that DSBs are repaired prior to the meiotic divisions. We show here that mutations in Drosophila genes required to process DSBs into crossovers delay two important steps in meiotic progression: a chromatin-remodeling process associated with DSB formation and the final steps of oocyte selection. Consistent with the hypothesis that a checkpoint has been activated, the delays in meiotic progression are suppressed by a mutation in the Drosophila homolog of pch2. The PCH2-dependent delays also require proteins thought to regulate the number and distribution of crossovers, suggesting that this checkpoint monitors events leading to crossover formation. Surprisingly, two lines of evidence suggest that the PCH2-dependent checkpoint does not reflect the accumulation of unprocessed recombination intermediates: the delays in meiotic progression do not depend on DSB formation or on mei-41, the Drosophila ATR homolog, which is required for the checkpoint response to unrepaired DSBs. We propose that the sites and/or conditions required to promote crossovers are established independently of DSB formation early in meiotic prophase. Furthermore, the PCH2-dependent checkpoint is activated by these events and pachytene progression is delayed until the DSB repair complexes required to generate crossovers are assembled. Interestingly, PCH2-dependent delays in prophase may allow additional crossovers to form.
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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.