ArticleNucleic acids research2018
A chromatin-associated protein required for inducing and limiting meiotic DNA double-strand break formation.
Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
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- A practical reference for studying meiosis in the model ciliateMarine life science & technology · 2022Review
- Zfp1, a Cys2His2 zinc finger protein is required for meiosis initiation inCell cycle (Georgetown, Tex.) · 2022Article
- PIWI-Directed DNA Elimination for Tetrahymena Genetics.Methods in molecular biology (Clifton, N.J.) · 2022Article
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- ATM controls meiotic DNA double-strand break formation and recombination and affects synaptonemal complex organization in plants.The Plant cell · 2021Article
- Tetrahymena meiosis: Simple yet ingenious.PLoS genetics · 2021Review
- Adhatoda Vasica attenuates inflammatory and hypoxic responses in preclinical mouse models: potential for repurposing in COVID-19-like conditions.Respiratory research · 2021Article
- Phospho-Regulation of Meiotic Prophase.Frontiers in cell and developmental biology · 2021Review
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- Spatial constraints on chromosomes are instrumental to meiotic pairing.Journal of cell science · 2020Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Programmed DNA double-strand breaks (DSBs) are required for meiotic recombination, but the number is strictly controlled because they are potentially harmful. Here we report a novel protein, Pars11, which is required for Spo11-dependent DSB formation in the protist Tetrahymena. Pars11 localizes to chromatin early in meiotic prophase in a Spo11-independent manner and is removed before the end of prophase. Pars11 removal depends on DSB formation and ATR-dependent phosphorylation. In the absence of the DNA damage sensor kinase ATR, Pars11 is retained on chromatin and excess DSBs are generated. Similar levels of Pars11 persistence and DSB overproduction occur in a non-phosphorylatable pars11 mutant. We conclude that Pars11 supports DSB formation by Spo11 until enough DSBs are formed; thereafter, DSB production stops in response to ATR-dependent degradation of Pars11 or its removal from chromatin. A similar DSB control mechanism involving a Rec114-Tel1/ATM-dependent negative feedback loop regulates DSB formation in budding yeast. However, there is no detectable sequence homology between Pars11 and Rec114, and DSB numbers are more tightly controlled by Pars11 than by Rec114. The discovery of this mechanism for DSB regulation in the evolutionarily distant protist and fungal lineages suggests that it is conserved across eukaryotes.
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Registered trials
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