ArticleNature communications2018
ATR is a multifunctional regulator of male mouse meiosis.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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Who cites it
39 citing papers in PubMed, 66 citations in OpenAlex.
- Tuning Meiotic Checkpoints: Evolutionary Costs and Mechanistic Trade-Offs.Annual review of genetics · 2026Review
- SYCP2 recruits HORMAD2 to chromosome axes for unsynapsed chromatin silencing and synapsis surveillance in meiosis.Nature communications · 2026Article
- Structure and function of the synaptonemal complex.The Journal of cell biology · 2026Review
- Genome-wide transcriptional silencing and mRNA stabilization allow the coordinated expression of the meiotic program in mice.Nucleic acids research · 2025Article
- Evolutionary innovations in germline biology of placental mammals identified by transcriptomics of first-wave spermatogenesis in opossum.Developmental cell · 2025Article
- The kinase ATR controls meiotic crossover distribution at the genome scale in Arabidopsis.The Plant cell · 2024Article
- Separable roles of the DNA damage response kinase Mec1ATR and its activator Rad24RAD17 during meiotic recombination.PLoS genetics · 2024Article
- A TOPBP1 allele causing male infertility uncouples XY silencing dynamics from sex body formation.eLife · 2024Article
- SRSF2 is required for mRNA splicing during spermatogenesis.BMC biology · 2023Article
- WNK1 is required during male pachynema to sustain fertility.iScience · 2023Article
- SPIDR is required for homologous recombination during mammalian meiosis.Nucleic acids research · 2023Article
- A-MYB and BRDT-dependent RNA Polymerase II pause release orchestrates transcriptional regulation in mammalian meiosis.Nature communications · 2023Article
- Genetic control of meiosis surveillance mechanisms in mammals.Frontiers in cell and developmental biology · 2023Review
- Active DNA damage response signaling initiates and maintains meiotic sex chromosome inactivation.Nature communications · 2022Article
- Characterization of 2,2',4,4'-tetrabromodiphenyl ether (BDE47)-induced testicular toxicity via single-cell RNA-sequencing.Precision clinical medicine · 2022Article
- Article
- Multiple 9-1-1 complexes promote homolog synapsis, DSB repair, and ATR signaling during mammalian meiosis.eLife · 2022Article
- Meiotic sex chromosome inactivation and the XY body: a phase separation hypothesis.Cellular and molecular life sciences : CMLS · 2021Review
- Proteome landscape and spatial map of mouse primordial germ cells.Science China. Life sciences · 2021Article
- Four-pronged negative feedback of DSB machinery in meiotic DNA-break control in mice.Nucleic acids research · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 5 institutions in 5 countries.
Funding
Abstract
Meiotic cells undergo genetic exchange between homologs through programmed DNA double-strand break (DSB) formation, recombination and synapsis. In mice, the DNA damage-regulated phosphatidylinositol-3-kinase-like kinase (PIKK) ATM regulates all of these processes. However, the meiotic functions of the PIKK ATR have remained elusive, because germline-specific depletion of this kinase is challenging. Here we uncover roles for ATR in male mouse prophase I progression. ATR deletion causes chromosome axis fragmentation and germ cell elimination at mid pachynema. This elimination cannot be rescued by deletion of ATM and the third DNA damage-regulated PIKK, PRKDC, consistent with the existence of a PIKK-independent surveillance mechanism in the mammalian germline. ATR is required for synapsis, in a manner genetically dissociable from DSB formation. ATR also regulates loading of recombinases RAD51 and DMC1 to DSBs and recombination focus dynamics on synapsed and asynapsed chromosomes. Our studies reveal ATR as a critical regulator of mouse 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.