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Regular Article |
a Department of Animal Breeding, Graduate School of Life and Agricultural Science and
b Department of Integrated Biosciences, Graduate School of Frontier Sciences, University of Tokyo, Bunkyo-ku, Tokyo 113-8657, Japan
c Department of Biology, University of Pennsylvania, Philadelphia, Pennsylvania 19104-6018
ABSTRACT
A shift from a meiotic cell cycle to a mitotic cell cycle occurs following fertilization. The molecular basis for this transition, however, is poorly understood. Although cyclin A1 is proposed to regulate M phase in the meiotic cell cycle, and cyclin A2 is proposed to regulate S and M phases in the mitotic cell cycle, little is known about changes in the expression levels of cyclin A1 and A2 during meiotic and mitotic cell cycles in mammalian oocytes. We report that the mRNA levels of both cyclins A1 and A2 decrease during oocyte maturation. The amount of cyclin A1 mRNA then increases between the one-cell and blastocyst stages, whereas that of cyclin A2 remains relatively constant. The amount of cyclin A1 protein declines during maturation and is not readily detected from the two-cell to the blastocyst stage. In contrast, cyclin A2 is not readily detected in the oocyte and metaphase II-arrested egg but is detected following fertilization and throughout the subsequent stages of preimplantation development. The appearance of cyclin A2 protein following fertilization positively correlates with an increase in the size of the mRNA. This increase, as well as the increase in the amount of cyclin A2 protein, is prevented by 3'-deoxyadenosine (3'-dA), an inhibitor of polyadenylation. Consistent with a role for cyclin A2 in regulating the G1/S transition, 3'-dA also inhibits DNA replication in treated one-cell embryos. These results suggest that regulation of expression of cyclins A1 and A2 is under posttranscriptional regulation and that the observed changes in their expression may be involved in the transformation of a meiotic cell cycle to a mitotic cell cycle following fertilization.
First decision: 11 April 2001.
1 This research was supported by a grant from the Ministry of Education, Science and Culture to F.A. and grant HD22681 from the National Institutes of Health to R.M.S.
2 Correspondence: Fugaku Aoki, Department of Animal Breeding, University of Tokyo, Yayoi 1-1-1, Bunkyo-ku, Tokyo 113-8657, Japan. FAX: 81 3 5841 8180; aokif{at}k.u-tokyo.ac.jp
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