减数分裂
微管
卵母细胞
细胞生物学
化学
动细胞
生物
胚胎
生物化学
基因
染色体
作者
Zhen Jin,Zhicai Zhang,Chen-Yu Xiao,Meiqi Li,Qianru Li,Leilei Gao
出处
期刊:Zygote
[Cambridge University Press]
日期:2023-12-04
卷期号:: 1-7
标识
DOI:10.1017/s0967199423000564
摘要
Summary Our previous studies have suggested that spastin, which aggregates on spindle microtubules in oocytes, may promote the assembly of mouse oocyte spindles by cutting microtubules. This action may be related to CRMP5, as knocking down CRMP5 results in reduced spindle microtubule density and maturation defects in oocytes. In this study, we found that, after knocking down CRMP5 in oocytes, spastin distribution shifted from the spindle to the spindle poles and errors in microtubule–kinetochore attachment appeared in oocyte spindles. However, CRMP5 did not interact with the other two microtubule-severing proteins, katanin-like-1 (KATNAL1) and fidgetin-like-1 (FIGNL1), which aggregate at the spindle poles. We speculate that, in oocytes, due to the reduction of spastin distribution on chromosomes after knocking down CRMP5, microtubule–kinetochore errors cannot be corrected through severing, resulting in meiotic division abnormalities and maturation defects in oocytes. This finding provides new insights into the regulatory mechanisms of spastin in oocytes and important opportunities for the study of meiotic division mechanisms.
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