ArticleMolecular and cellular biology2005
Surveillance of different recombination defects in mouse spermatocytes yields distinct responses despite elimination at an identical developmental stage.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 papers.
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Who cites it
136 citing papers in PubMed, 237 citations in OpenAlex.
- SYCP2 recruits HORMAD2 to chromosome axes for unsynapsed chromatin silencing and synapsis surveillance in meiosis.Nature communications · 2026Article
- The transcription factor E4F1 is crucial for spermatogonial differentiation and meiosis progression in mice.BMC genomics · 2026Article
- Meiotic Recombination in Teleosts.Advances in experimental medicine and biology · 2026Review
- HEIP1 orchestrates pro-crossover protein activity during mammalian meiosis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Distinct cellular and reproductive consequences of meiotic chromosome synapsis defects in syce2 and sycp1 mutant zebrafish.PLoS genetics · 2025Article
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- hnRNPC Functions with HuR to Regulate Alternative Splicing in an m6A-Dependent Manner and is Essential for Meiosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Genome-wide transcriptional silencing and mRNA stabilization allow the coordinated expression of the meiotic program in mice.Nucleic acids research · 2025Article
- Intercellular bridges are essential for transposon repression and meiosis in the male germline.Nature communications · 2025Article
- Protein disulfide isomerase is essential for spermatogenesis in mice.JCI insight · 2024Article
- Seeding the meiotic DNA break machinery and initiating recombination on chromosome axes.Nature communications · 2024Article
- TAF7L regulates early stages of male germ cell development in the rat.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Essential roles of the ANKRD31-REC114 interaction in meiotic recombination and mouse spermatogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- The proper interplay between the expression of Spo11 splice isoforms and the structure of the pseudoautosomal region promotes XY chromosomes recombination.Cellular and molecular life sciences : CMLS · 2023Article
- GCNA is a histone binding protein required for spermatogonial stem cell maintenance.Nucleic acids research · 2023Article
- Age-related elevation of O-GlcNAc causes meiotic arrest in male mice.Cell death discovery · 2023Article
- The RNA-binding protein FUS/TLS interacts with SPO11 and PRDM9 and localize at meiotic recombination hotspots.Cellular and molecular life sciences : CMLS · 2023Article
- Pre-meiotic deletion of PEX5 causes spermatogenesis failure and infertility in mice.Cell proliferation · 2023Article
- Genetic control of meiosis surveillance mechanisms in mammals.Frontiers in cell and developmental biology · 2023Review
76 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Fundamentally different recombination defects cause apoptosis of mouse spermatocytes at the same stage in development, stage IV of the seminiferous epithelium cycle, equivalent to mid-pachynema in normal males. To understand the cellular response(s) that triggers apoptosis, we examined markers of spermatocyte development in mice with different recombination defects. In Spo11(-)(/)(-) mutants, which lack the double-strand breaks (DSBs) that initiate recombination, spermatocytes express markers of early to mid-pachynema, forming chromatin domains that contain sex body-associated proteins but that rarely encompass the sex chromosomes. Dmc1(-)(/)(-) spermatocytes, impaired in DSB repair, appear to arrest at or about late zygonema. Epistasis analysis reveals that this earlier arrest is a response to unrepaired DSBs, and cytological analysis implicates the BRCT-containing checkpoint protein TOPBP1. Atm(-)(/)(-) spermatocytes show similarities to Dmc1(-)(/)(-) spermatocytes, suggesting that ATM promotes meiotic DSB repair. Msh5(-)(/)(-) mutants display a set of characteristics distinct from these other mutants. Thus, despite equivalent stages of spermatocyte elimination, different recombination-defective mutants manifest distinct responses, providing insight into surveillance mechanisms in male meiosis.
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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.