ArticlePLoS genetics2008
ATM promotes the obligate XY crossover and both crossover control and chromosome axis integrity on autosomes.
Article in PLoS genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
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Who cites it
80 citing papers in PubMed, 115 citations in OpenAlex.
- Tuning Meiotic Checkpoints: Evolutionary Costs and Mechanistic Trade-Offs.Annual review of genetics · 2026Review
- NSMCE2 dispensability in mouse spermatogenesis suggests functional redundancy within the meiotic repair network.Frontiers in cell and developmental biology · 2026Article
- Neo-sex Chromosomes Track the Mitochondrial Phylogeny and Exhibit an Extensive Added Stratum of Recombination Suppression in Honeyeaters (Aves: Meliphagidae).Genome biology and evolution · 2025Article
- Mismatch repair disturbs meiotic crossover control in S. cerevisiae.Nucleic acids research · 2025Article
- A comparison of spermatogenesis between flies and men-conserved processes of male gamete production.Human reproduction update · 2025Review
- Molecular characterization and expression ofVeterinary and animal science · 2025Review
- Separable roles of the DNA damage response kinase Mec1ATR and its activator Rad24RAD17 during meiotic recombination.PLoS genetics · 2024Article
- Recent advances in mechanisms ensuring the pairing, synapsis and segregation of XY chromosomes in mice and humans.Cellular and molecular life sciences : CMLS · 2024Review
- Computational Tools for the Analysis of Meiotic Prophase I Images.Methods in molecular biology (Clifton, N.J.) · 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
- Stepwise recombination suppression around the mating-type locus in an ascomycete fungus with self-fertile spores.PLoS genetics · 2023Article
- Genetic control of meiosis surveillance mechanisms in mammals.Frontiers in cell and developmental biology · 2023Review
- p53 Controls Meiotic Prophase Progression and Crossover Formation.International journal of molecular sciences · 2022Article
- SCF ubiquitin E3 ligase regulates DNA double-strand breaks in early meiotic recombination.Nucleic acids research · 2022Article
- RAD51 is essential for spermatogenesis and male fertility in mice.Cell death discovery · 2022Article
- CRISPR-Cas9 effectors facilitate generation of single-sex litters and sex-specific phenotypes.Nature communications · 2021Article
- Non-Coding RNAs and Splicing Activity in Testicular Germ Cell Tumors.Life (Basel, Switzerland) · 2021Review
- ATM controls meiotic DNA double-strand break formation and recombination and affects synaptonemal complex organization in plants.The Plant cell · 2021Article
- Paternal USP26 mutations raise Klinefelter syndrome risk in the offspring of mice and humans.The EMBO journal · 2021Article
- Four-pronged negative feedback of DSB machinery in meiotic DNA-break control in mice.Nucleic acids research · 2021Article
20 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 2 countries.
Funding
Abstract
During meiosis in most sexually reproducing organisms, recombination forms crossovers between homologous maternal and paternal chromosomes and thereby promotes proper chromosome segregation at the first meiotic division. The number and distribution of crossovers are tightly controlled, but the factors that contribute to this control are poorly understood in most organisms, including mammals. Here we provide evidence that the ATM kinase or protein is essential for proper crossover formation in mouse spermatocytes. ATM deficiency causes multiple phenotypes in humans and mice, including gonadal atrophy. Mouse Atm-/- spermatocytes undergo apoptosis at mid-prophase of meiosis I, but Atm(-/-) meiotic phenotypes are partially rescued by Spo11 heterozygosity, such that ATM-deficient spermatocytes progress to meiotic metaphase I. Strikingly, Spo11+/-Atm-/- spermatocytes are defective in forming the obligate crossover on the sex chromosomes, even though the XY pair is usually incorporated in a sex body and is transcriptionally inactivated as in normal spermatocytes. The XY crossover defect correlates with the appearance of lagging chromosomes at metaphase I, which may trigger the extensive metaphase apoptosis that is observed in these cells. In addition, control of the number and distribution of crossovers on autosomes appears to be defective in the absence of ATM because there is an increase in the total number of MLH1 foci, which mark the sites of eventual crossover formation, and because interference between MLH1 foci is perturbed. The axes of autosomes exhibit structural defects that correlate with the positions of ongoing recombination. Together, these findings indicate that ATM plays a role in both crossover control and chromosome axis integrity and further suggests that ATM is important for coordinating these features of meiotic chromosome dynamics.
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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.