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Interplay between Pds5 and Rec8 in regulating chromosome axis length and crossover frequency

Meiotic chromosomes have a loop/axis architecture, with axis length determining crossover frequency. Meiosis-specific Pds5 depletion mutants have shorter chromosome axes and lower homologous chromosome pairing and recombination frequency. However, it is poorly understood how Pds5 coordinately regula...

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Detalles Bibliográficos
Autores principales: Song, Meihui, Zhai, Binyuan, Yang, Xiao, Tan, Taicong, Wang, Ying, Yang, Xuan, Tan, Yingjin, Chu, Tingting, Cao, Yanding, Song, Yulong, Wang, Shunxin, Zhang, Liangran
Formato: Online Artículo Texto
Lenguaje:English
Publicado: American Association for the Advancement of Science 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7954452/
https://www.ncbi.nlm.nih.gov/pubmed/33712462
http://dx.doi.org/10.1126/sciadv.abe7920
Descripción
Sumario:Meiotic chromosomes have a loop/axis architecture, with axis length determining crossover frequency. Meiosis-specific Pds5 depletion mutants have shorter chromosome axes and lower homologous chromosome pairing and recombination frequency. However, it is poorly understood how Pds5 coordinately regulates these processes. In this study, we show that only ~20% of wild-type level of Pds5 is required for homolog pairing and that higher levels of Pds5 dosage-dependently regulate axis length and crossover frequency. Moderate changes in Pds5 protein levels do not explicitly impair the basic recombination process. Further investigations show that Pds5 does not regulate chromosome axes by altering Rec8 abundance. Conversely, Rec8 regulates chromosome axis length by modulating Pds5. These findings highlight the important role of Pds5 in regulating meiosis and its relationship with Rec8 to regulate chromosome axis length and crossover frequency with implications for evolutionary adaptation.