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Proline-rich protein PRR19 functions with cyclin-like CNTD1 to promote meiotic crossing over in mouse

Author

Listed:
  • Anastasiia Bondarieva

    (Technische Universität Dresden)

  • Kavya Raveendran

    (Technische Universität Dresden)

  • Vladyslav Telychko

    (Technische Universität Dresden)

  • H. B. D. Prasada Rao

    (University of California Davis
    University of California Davis)

  • Ramya Ravindranathan

    (Technische Universität Dresden)

  • Chrysoula Zorzompokou

    (Technische Universität Dresden)

  • Friederike Finsterbusch

    (Technische Universität Dresden)

  • Ihsan Dereli

    (Technische Universität Dresden)

  • Frantzeskos Papanikos

    (Technische Universität Dresden)

  • Daniel Tränkner

    (Technische Universität Dresden)

  • Alexander Schleiffer

    (Research Institute of Molecular Pathology (IMP)
    Institute of Molecular Biotechnology (IMBA))

  • Ji-Feng Fei

    (South China Normal University)

  • Anna Klimova

    (National Center for Tumor Diseases (NCT)
    Technische Universität Dresden)

  • Masaru Ito

    (University of California Davis
    University of California Davis)

  • Dhananjaya S. Kulkarni

    (University of California Davis
    University of California Davis)

  • Ingo Roeder

    (National Center for Tumor Diseases (NCT)
    Technische Universität Dresden)

  • Neil Hunter

    (University of California Davis
    University of California Davis
    University of California Davis)

  • Attila Tóth

    (Technische Universität Dresden)

Abstract

Orderly chromosome segregation is enabled by crossovers between homologous chromosomes in the first meiotic division. Crossovers arise from recombination-mediated repair of programmed DNA double-strand breaks (DSBs). Multiple DSBs initiate recombination, and most are repaired without crossover formation, although one or more generate crossovers on each chromosome. Although the underlying mechanisms are ill-defined, the differentiation and maturation of crossover-specific recombination intermediates requires the cyclin-like CNTD1. Here, we identify PRR19 as a partner of CNTD1. We find that, like CNTD1, PRR19 is required for timely DSB repair and the formation of crossover-specific recombination complexes. PRR19 and CNTD1 co-localise at crossover sites, physically interact, and are interdependent for accumulation, indicating a PRR19-CNTD1 partnership in crossing over. Further, we show that CNTD1 interacts with a cyclin-dependent kinase, CDK2, which also accumulates in crossover-specific recombination complexes. Thus, the PRR19-CNTD1 complex may enable crossover differentiation by regulating CDK2.

Suggested Citation

  • Anastasiia Bondarieva & Kavya Raveendran & Vladyslav Telychko & H. B. D. Prasada Rao & Ramya Ravindranathan & Chrysoula Zorzompokou & Friederike Finsterbusch & Ihsan Dereli & Frantzeskos Papanikos & D, 2020. "Proline-rich protein PRR19 functions with cyclin-like CNTD1 to promote meiotic crossing over in mouse," Nature Communications, Nature, vol. 11(1), pages 1-20, December.
    • Handle: RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-16885-3
    DOI: 10.1038/s41467-020-16885-3
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    Cited by:

    1. Ihsan Dereli & Vladyslav Telychko & Frantzeskos Papanikos & Kavya Raveendran & Jiaqi Xu & Michiel Boekhout & Marcello Stanzione & Benjamin Neuditschko & Naga Sailaja Imjeti & Elizaveta Selezneva & Has, 2024. "Seeding the meiotic DNA break machinery and initiating recombination on chromosome axes," Nature Communications, Nature, vol. 15(1), pages 1-23, December.

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