Journal
JOURNAL OF CELLULAR PHYSIOLOGY
Volume 237, Issue 1, Pages 730-742Publisher
WILEY
DOI: 10.1002/jcp.30498
Keywords
APC; C-CDC20; germinal vesicle breakdown; meiosis; oocyte; Septin 4
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Funding
- National Natural Science Foundation of China [31530049]
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The study indicates that Septin 4 plays a crucial role in regulating the G2/M transition in mouse oocytes by controlling the accumulation of CCNB1. Depletion of Septin 4 leads to GV arrest and alters the expression level of CDC20, while there is no significant change in the expression level of CDH1.
In mammals, oocytes are arrested at G2/prophase for a long time, which is called germinal vesicle (GV) arrest. After puberty, fully-grown oocytes are stimulated by a gonadotropin surge to resume meiosis as indicated by GV breakdown (GVBD). CCNB1 is accumulated to a threshold level to trigger the activation of maturation promoting factor (MPF), inducing the G2/M transition. It is generally recognized that the anaphase-promoting complex/cyclosome (APC/C) and its cofactor CDH1 (also known as FZR1) regulates the accumulation/degradation of CCNB1. Here, by using small interfering RNA (siRNA) and messenger RNA (mRNA) microinjection, immunofluorescence and confocal microscopy, immunoprecipitation, time-lapse live imaging, and immunoblotting analysis, we showed that Septin 4 regulates the G2/M transition by regulating the accumulation of CCNB1 via APC/C-CDC20. Depletion of Septin 4 caused GV arrest by reducing CCNB1 accumulation. Unexpectedly, the expression level of CDC20 was higher in Septin 4 siRNA-injected oocytes than in control oocytes, but there was no significant change in the expression level of CDH1. Importantly, the reduced GVBD after Septin 4 depletion could be rescued not only by over-expressing CCNB1 but also could be partially rescued by depleting CDC20. Taken together, our results demonstrate that Septin 4 may play a critical role in meiotic G2/M transition by indirect regulation of CCNB1 stabilization in mouse oocytes.
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