دورية أكاديمية
أعرض في EDS

Four-pronged negative feedback of DSB machinery in meiotic DNA-break control in mice.

التفاصيل البيبلوغرافية
العنوان: Four-pronged negative feedback of DSB machinery in meiotic DNA-break control in mice.
المؤلفون: Dereli I; Institute of Physiological Chemistry, Faculty of Medicine at the TU Dresden, Fiedlerstrasse 42, 01307 Dresden, Germany., Stanzione M; Institute of Physiological Chemistry, Faculty of Medicine at the TU Dresden, Fiedlerstrasse 42, 01307 Dresden, Germany., Olmeda F; Max Planck Institute for the Physics of Complex Systems, Noethnitzer Strasse 38, 01187 Dresden, Germany., Papanikos F; Institute of Physiological Chemistry, Faculty of Medicine at the TU Dresden, Fiedlerstrasse 42, 01307 Dresden, Germany., Baumann M; Institute of Physiological Chemistry, Faculty of Medicine at the TU Dresden, Fiedlerstrasse 42, 01307 Dresden, Germany., Demir S; Institute of Physiological Chemistry, Faculty of Medicine at the TU Dresden, Fiedlerstrasse 42, 01307 Dresden, Germany., Carofiglio F; Department of Developmental Biology, Erasmus MC - University Medical Center, Rotterdam, The Netherlands., Lange J; Molecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.; Howard Hughes Medical Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA., de Massy B; Institute of Human Genetics, UMR 9002, CNRS, Université de Montpellier, 34396 Montpellier cedex 5, France., Baarends WM; Department of Developmental Biology, Erasmus MC - University Medical Center, Rotterdam, The Netherlands., Turner J; Sex Chromosome Biology Laboratory, The Francis Crick Institute, London, NW1 1AT, UK., Rulands S; Max Planck Institute for the Physics of Complex Systems, Noethnitzer Strasse 38, 01187 Dresden, Germany.; Center for Systems Biology Dresden (CSBD), Pfotenhauer Strasse 108, 01307 Dresden, Germany., Tóth A; Institute of Physiological Chemistry, Faculty of Medicine at the TU Dresden, Fiedlerstrasse 42, 01307 Dresden, Germany.
المصدر: Nucleic acids research [Nucleic Acids Res] 2021 Mar 18; Vol. 49 (5), pp. 2609-2628.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Oxford University Press Country of Publication: England NLM ID: 0411011 Publication Model: Print Cited Medium: Internet ISSN: 1362-4962 (Electronic) Linking ISSN: 03051048 NLM ISO Abbreviation: Nucleic Acids Res Subsets: MEDLINE
أسماء مطبوعة: Publication: 1992- : Oxford : Oxford University Press
Original Publication: London, Information Retrieval ltd.
مواضيع طبية MeSH: DNA Breaks, Double-Stranded*, Meiosis/*genetics, ATPases Associated with Diverse Cellular Activities/physiology ; Animals ; Ataxia Telangiectasia Mutated Proteins/metabolism ; Cell Cycle Proteins/physiology ; Chromosome Pairing ; Feedback, Physiological ; Gametogenesis ; Mice ; Pachytene Stage ; Sex Chromosomes ; Signal Transduction
مستخلص: In most taxa, halving of chromosome numbers during meiosis requires that homologous chromosomes (homologues) pair and form crossovers. Crossovers emerge from the recombination-mediated repair of programmed DNA double-strand breaks (DSBs). DSBs are generated by SPO11, whose activity requires auxiliary protein complexes, called pre-DSB recombinosomes. To elucidate the spatiotemporal control of the DSB machinery, we focused on an essential SPO11 auxiliary protein, IHO1, which serves as the main anchor for pre-DSB recombinosomes on chromosome cores, called axes. We discovered that DSBs restrict the DSB machinery by at least four distinct pathways in mice. Firstly, by activating the DNA damage response (DDR) kinase ATM, DSBs restrict pre-DSB recombinosome numbers without affecting IHO1. Secondly, in their vicinity, DSBs trigger IHO1 depletion mainly by another DDR kinase, ATR. Thirdly, DSBs enable homologue synapsis, which promotes the depletion of IHO1 and pre-DSB recombinosomes from synapsed axes. Finally, DSBs and three DDR kinases, ATM, ATR and PRKDC, enable stage-specific depletion of IHO1 from all axes. We hypothesize that these four negative feedback pathways protect genome integrity by ensuring that DSBs form without excess, are well-distributed, and are restricted to genomic locations and prophase stages where DSBs are functional for promoting homologue pairing and crossover formation.
(© The Author(s) 2021. Published by Oxford University Press on behalf of Nucleic Acids Research.)
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معلومات مُعتمدة: P30 CA008748 United States CA NCI NIH HHS; R35 GM118092 United States GM NIGMS NIH HHS; FC001193 United Kingdom CRUK_ Cancer Research UK; FC001193 United Kingdom WT_ Wellcome Trust; United States HHMI Howard Hughes Medical Institute; FC001193 United Kingdom MRC_ Medical Research Council
المشرفين على المادة: 0 (Cell Cycle Proteins)
EC 2.7.1.- (Atr protein, mouse)
EC 2.7.11.1 (Ataxia Telangiectasia Mutated Proteins)
EC 3.6.4.- (ATPases Associated with Diverse Cellular Activities)
EC 3.6.4.- (Trip13 protein, mouse)
تواريخ الأحداث: Date Created: 20210223 Date Completed: 20210326 Latest Revision: 20220129
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC7969012
DOI: 10.1093/nar/gkab082
PMID: 33619545
قاعدة البيانات: MEDLINE
الوصف
تدمد:1362-4962
DOI:10.1093/nar/gkab082