ArticlePLoS genetics2010
Mouse TRIP13/PCH2 is required for recombination and normal higher-order chromosome structure during meiosis.
Article in PLoS genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 129 papers, 1 of them a synthesis that pooled it.
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Who cites it
129 citing papers in PubMed, 1 synthesis or guideline pooled it, 212 citations in OpenAlex.
- Pooled it
- Meiotic pairing through barcode-like satellite DNA repeats.Nature communications · 2026Article
- Neddylation is indispensable for early meiotic progression in spermatocytes via destabilizing HORMAD1 by SCF ubiquitin E3 ligase during synapsis.Cell & bioscience · 2026Article
- Melatonin suppresses cancer cell proliferation, DNA repair and expression of the oncogene TRIP13.Cell death discovery · 2025Article
- TRIP13 fosters both transcriptional silencing and DSB repair during meiosis.bioRxiv : the preprint server for biology · 2025Article
- Article
- Aberrant activation of chromosome asynapsis checkpoint triggers oocyte elimination.Nature communications · 2025Article
- Article
- Repeated ionizing radiation exposure induces TRIP13 expression, conferring radioresistance in lung cancer cells.Scientific reports · 2025Article
- The conserved ATPase PCH-2 controls the number and distribution of crossovers by antagonizing their formation inbioRxiv : the preprint server for biology · 2024Article
- TRIP13: A promising cancer immunotherapy target.Cancer innovation · 2024Review
- Identification of a novel splicing variant of thyroid hormone receptor interaction protein 13 (TRIP13) in female infertility characterized by oocyte maturation arrest.Journal of assisted reproduction and genetics · 2024Article
- TRIP13 localizes to synapsed chromosomes and functions as a dosage-sensitive regulator of meiosis.eLife · 2024Article
- TRIP13 regulates progression of gastric cancer through stabilising the expression of DDX21.Cell death & disease · 2024Article
- BRCA1 safeguards genome integrity by activating chromosome asynapsis checkpoint to eliminate recombination-defective oocytes.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The N-terminal modification of HORMAD2 causes its ectopic persistence on synapsed chromosomes without meiotic blockade.Reproduction (Cambridge, England) · 2024Article
- [TRIP13 Enhances Radioresistance of Lung Adenocarcinoma Cells through the Homologous Recombination Pathway].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2024Article
- Germline specific genes increase DNA double-strand break repair and radioresistance in lung adenocarcinoma cells.Cell death & disease · 2024Article
- TI17, a novel compound, exerts anti-MM activity by impairing Trip13 function of DSBs repair and enhancing DNA damage.Cancer medicine · 2023Article
- The novel norcantharidin derivative DCZ5417 suppresses multiple myeloma progression by targeting the TRIP13-MAPK-YWHAE signaling pathway.Journal of translational medicine · 2023Article
69 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
6 authors at 3 institutions in 3 countries.
Funding
Abstract
Accurate chromosome segregation during meiosis requires that homologous chromosomes pair and become physically connected so that they can orient properly on the meiosis I spindle. These connections are formed by homologous recombination closely integrated with the development of meiosis-specific, higher-order chromosome structures. The yeast Pch2 protein has emerged as an important factor with roles in both recombination and chromosome structure formation, but recent analysis suggested that TRIP13, the mouse Pch2 ortholog, is not required for the same processes. Using distinct Trip13 alleles with moderate and severe impairment of TRIP13 function, we report here that TRIP13 is required for proper synaptonemal complex formation, such that autosomal bivalents in Trip13-deficient meiocytes frequently displayed pericentric synaptic forks and other defects. In males, TRIP13 is required for efficient synapsis of the sex chromosomes and for sex body formation. Furthermore, the numbers of crossovers and chiasmata are reduced in the absence of TRIP13, and their distribution along the chromosomes is altered, suggesting a role for TRIP13 in aspects of crossover formation and/or control. Recombination defects are evident very early in meiotic prophase, soon after DSB formation. These findings provide evidence for evolutionarily conserved functions for TRIP13/Pch2 in both recombination and formation of higher order chromosome structures, and they support the hypothesis that TRIP13/Pch2 participates in coordinating these key aspects of meiotic chromosome behavior.
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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.