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

Anastasiia Bondarieva, Kavya Raveendran, Vladyslav Telychko, H. B. D. Prasada Rao, Ramya Ravindranathan, Chrysoula Zorzompokou, Friederike Finsterbusch, Ihsan Dereli, Frantzeskos Papanikos, Daniel Tränkner, Alexander Schleiffer, Ji-Feng Fei, Anna Klimova, Masaru Ito, Dhananjaya S. Kulkarni, Ingo Roeder, Neil Hunter and Attila Tóth ()
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Anastasiia Bondarieva: Technische Universität Dresden
Kavya Raveendran: Technische Universität Dresden
Vladyslav Telychko: Technische Universität Dresden
H. B. D. Prasada Rao: 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)
Ji-Feng Fei: South China Normal University
Anna Klimova: National Center for Tumor Diseases (NCT)
Masaru Ito: University of California Davis
Dhananjaya S. Kulkarni: University of California Davis
Ingo Roeder: National Center for Tumor Diseases (NCT)
Neil Hunter: University of California Davis
Attila Tóth: Technische Universität Dresden

Nature Communications, 2020, vol. 11, issue 1, 1-20

Abstract: 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.

Date: 2020
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DOI: 10.1038/s41467-020-16885-3

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