TY - JOUR
T1 - Proline-rich protein PRR19 functions with cyclin-like CNTD1 to promote meiotic crossing over in mouse
AU - Bondarieva, Anastasiia
AU - Raveendran, Kavya
AU - Telychko, Vladyslav
AU - Rao, H. B.D.Prasada
AU - Ravindranathan, Ramya
AU - Zorzompokou, Chrysoula
AU - Finsterbusch, Friederike
AU - Dereli, Ihsan
AU - Papanikos, Frantzeskos
AU - Tränkner, Daniel
AU - Schleiffer, Alexander
AU - Fei, Ji Feng
AU - Klimova, Anna
AU - Ito, Masaru
AU - Kulkarni, Dhananjaya S.
AU - Roeder, Ingo
AU - Hunter, Neil
AU - Tóth, Attila
PY - 2020/12/1
Y1 - 2020/12/1
N2 - 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.
AB - 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.
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U2 - 10.1038/s41467-020-16885-3
DO - 10.1038/s41467-020-16885-3
M3 - Article
C2 - 32555348
AN - SCOPUS:85086690993
VL - 11
JO - Nature Communications
JF - Nature Communications
SN - 2041-1723
IS - 1
M1 - 3101
ER -