ArticleGenetics2011
Pch2 modulates chromatid partner choice during meiotic double-strand break repair in Saccharomyces cerevisiae.
Article in Genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 47 citations in OpenAlex.
- AAA ATPase TRIP13 is overexpressed in prostate cancer and promotes tumor progression.Translational oncology · 2026Article
- Melatonin suppresses cancer cell proliferation, DNA repair and expression of the oncogene TRIP13.Cell death discovery · 2025Article
- The ATPase activity of yeast chromosome axis protein Hop1 affects the frequency of meiotic crossovers.Nucleic acids research · 2025Article
- Repeated ionizing radiation exposure induces TRIP13 expression, conferring radioresistance in lung cancer cells.Scientific reports · 2025Article
- Role of TRIP13 in human cancer development.Molecular biology reports · 2024Review
- PCH-2 and meiotic HORMADs: A module for evolutionary innovation in meiosis?Current topics in developmental biology · 2023Review
- Chromosome architecture and homologous recombination in meiosis.Frontiers in cell and developmental biology · 2022Review
- Meiotic chromosome axis remodelling is critical for meiotic recombination in Brassica rapa.Journal of experimental botany · 2021Article
- TRIP13 promotes the proliferation and invasion of lung cancer cells via the Wnt signaling pathway and epithelial-mesenchymal transition.Journal of molecular histology · 2021Article
- A pathway for error-free non-homologous end joining of resected meiotic double-strand breaks.Nucleic acids research · 2021Article
- PCH-2 collaborates with CMT-1 to proofread meiotic homolog interactions.PLoS genetics · 2020Article
- Article
- Characterization of Pch2 localization determinants reveals a nucleolar-independent role in the meiotic recombination checkpoint.Chromosoma · 2019Article
- Persistent DNA-break potential near telomeres increases initiation of meiotic recombination on short chromosomes.Nature communications · 2019Article
- Insights into a Crucial Role of TRIP13 in Human Cancer.Computational and structural biotechnology journal · 2019Review
- Article
- Modulating Crossover Frequency and Interference for Obligate Crossovers inG3 (Bethesda, Md.) · 2017Article
- TRIP13 impairs mitotic checkpoint surveillance and is associated with poor prognosis in multiple myeloma.Oncotarget · 2017Article
- Prevention of DNA Rereplication Through a Meiotic Recombination Checkpoint Response.G3 (Bethesda, Md.) · 2016Article
- The Pch2 AAA+ ATPase promotes phosphorylation of the Hop1 meiotic checkpoint adaptor in response to synaptonemal complex defects.Nucleic acids research · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
In most organisms, the segregation of chromosomes during the first meiotic division is dependent upon at least one crossover (CO) between each pair of homologous chromosomes. COs can result from chromosome double-strand breaks (DSBs) that are induced and preferentially repaired using the homologous chromosome as a template. The PCH2 gene of budding yeast is required to establish proper meiotic chromosome axis structure and to regulate meiotic interhomolog DSB repair outcomes. These roles appear conserved in the mouse ortholog of PCH2, Trip13, which is also involved in meiotic chromosome axis organization and the regulation of DSB repair. Using a combination of genetic and physical assays to monitor meiotic DSB repair, we present data consistent with pch2Δ mutants showing defects in suppressing intersister DSB repair. These defects appear most pronounced in dmc1Δ mutants, which are defective for interhomolog repair, and explain the previously reported observation that pch2Δ dmc1Δ cells can complete meiosis. Results from genetic epistasis analyses involving spo13Δ, rad54Δ, and mek1/MEK1 alleles and an intersister recombination reporter assay are also consistent with Pch2 acting to limit intersister repair. We propose a model in which Pch2 is required to promote full Mek1 activity and thereby promotes interhomolog repair.
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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.