ArticlePLoS genetics2025
Tel1 is recruited at chromosomal loop/axis contact sites to modulate meiotic DNA double-strand breaks interference.
Article in PLoS genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- MRE11 suppresses germline mutagenesis at meiotic double-strand breaks in mice.Genes & development · 2026Article
- MRE11 suppresses germline mutagenesis at meiotic double-strand breaks in mice.bioRxiv : the preprint server for biology · 2026Article
- Mutual, spatially limited control of meiotic DNA break formation by Mre11-Rad50-Nbs1 DNA repair complex and Tel1 (ATM) protein kinase.Nucleic acids research · 2025Article
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During meiosis, the programmed formation of DNA double-strand breaks (DSBs) by Spo11, a conserved topoisomerase VI family protein, initiates homologous recombination that leads to crossovers between homologous chromosomes, essential for accurate chromosome segregation and genome evolution. The DSB number, distribution and timing of formation are regulated during meiosis to ensure crossing over on all chromosomes and prevent genome instability. In S. cerevisiae, DSB interference suppresses the coincident formation of DSBs in neighboring hotspots through a Tel1/ATM dependent mechanism that remains unexplored. Here, we demonstrate that Tel1 is recruited to meiotic DSB hotspots and chromosomal axis sites in a DSB-dependent manner. This supports the tethered loop-axis complex (TLAC) model that postulates meiotic DSBs are formed within the chromosome axis environment. Tel1 recruitment to meiotic DSBs, DSB interference and the meiotic DNA damage checkpoint are all dependent on the C-terminal moiety of Xrs2, known to mediate Tel1-Xrs2 interaction in vegetative cells. However, mutation of the Xrs2 FxF/Y motif, known to stabilize Tel1 interaction with Xrs2, does not affect DSBs interference but abolishes the Tel1-dependent DNA damage checkpoint. Altogether, this work uncovers the dynamic association of Tel1 with meiotic chromosomes and highlights the critical role of its interaction with Xrs2 in fine-tuning both the meiotic DNA damage checkpoint and DSB interference.
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