Song Meihui, Zhai Binyuan, Yang Xiao, Tan Taicong, Wang Ying, Yang Xuan, Tan Yingjin, Chu Tingting, Cao Yanding, Song Yulong, Wang Shunxin, Zhang Liangran
Center for Reproductive Medicine, Cheeloo College of Medicine, State Key Laboratory of Microbial Technology, Shandong University, Jinan, Shandong 250012, China.
Key Laboratory of Reproductive Endocrinology of Ministry of Education, Jinan, Shandong 250001, China.
Sci Adv. 2021 Mar 12;7(11). doi: 10.1126/sciadv.abe7920. Print 2021 Mar.
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.
减数分裂染色体具有环状/轴状结构,轴的长度决定交叉频率。减数分裂特异性Pds5缺失突变体的染色体轴较短,同源染色体配对和重组频率较低。然而,人们对Pds5如何协调调节这些过程知之甚少。在本研究中,我们表明同源配对仅需要约20%野生型水平的Pds5,并且更高水平的Pds5剂量依赖性地调节轴长度和交叉频率。Pds5蛋白水平的适度变化不会明显损害基本的重组过程。进一步研究表明,Pds5不会通过改变Rec8丰度来调节染色体轴。相反,Rec8通过调节Pds5来调节染色体轴长度。这些发现突出了Pds5在调节减数分裂中的重要作用及其与Rec8在调节染色体轴长度和交叉频率方面的关系,对进化适应具有重要意义。