The Role of RhoA in the Germinal Vesicle Breakdown of Mouse Oocytes

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Title
The Role of RhoA in the Germinal Vesicle Breakdown of Mouse Oocytes
Author(s)
Yong Pil Cheon; Sung Woo Kim; Soo Jung Kim; Young Il Yeom; Chae Joon Cheong; Kwon Soo Ha
Bibliographic Citation
Biochemical and Biophysical Research Communications, vol. 273, no. 3, pp. 997-1002
Publication Year
2000
Abstract
We have investigated a new role of RhoA in the germinal vesicle breakdown (GVBD) of mouse oocytes. First, RhoA was identified by immunostaining and ADP-ribosylation in germinal vesicle (GV) stage-oocytes. RhoA was mainly localized in the ooplasmic area, but rarely detected in germinal vesicle. Incubation of oocyte extract with C3 transferase induced a strong ADP-ribosylation at about 25 kDa. Incubation of GV-stage oocytes in culture medium induced the spontaneous maturation to GVBD by about 78 and 87% of total oocytes at 1 and 3 h, respectively. However, microinjection of C3 transferase into GV-stage oocytes significantly inhibited GVBD at 1 (GVBD = 29%) and 3 h (GVBD = 49%). To study the role of reactive oxygen species (ROS) in the oocyte maturation, the level of intra-oocyte ROS was measured using a ROS-specific fluorescent dye H2DCFDA during the oocyte maturation. Spontaneous maturation of GV-stage oocytes induced a significant increase of ROS at 3 h by about twofold over the control level and then the increased level was maintained until 6 h. However, microinjection of C3 transferase inhibited the production of intra-oocyte ROS. Incubation with ROS scavengers, N-acetyl-L-cysteine and catalase, blocked the ROS increase. The ROS scavengers also significantly inhibited GVBD, as did C3 transferase. Thus, it was proposed that RhoA was involved in the GVBD, possibly by the production of ROS in mouse oocytes.
Keyword
mouse oocyteRhoAreactive oxygen speciesC3 transferaseGVBD
ISSN
0006-291X
Publisher
Elsevier
DOI
http://dx.doi.org/10.1006/bbrc.2000.3052
Type
Article
Appears in Collections:
Division of Biomedical Research > Personalized Genomic Medicine Research Center > 1. Journal Articles
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