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First published online 18 January 2006
doi: 10.1242/dev.02241
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1 Laboratory of Biochemistry and Genetics, National Institute of Diabetes and
Digestive and Kidney Diseases, National Institutes of Health, 8 Center Drive,
Building 8, Room 323, Bethesda, MD 20892, USA.
2 Department of Cell Biology, Vanderbilt University School of Medicine,
Nashville, TN 37232-2175, USA.
3 Department of Molecular Genetics, University of Texas, M. D. Anderson Cancer
Center, Houston, TX 77030, USA.
Author for correspondence (e-mail:
andyg{at}intra.niddk.nih.gov)
Accepted 7 December 2005
Maturation promoting factor (MPF), a complex of cyclin-dependent kinase 1 and cyclin B, drives oocyte maturation in all animals. Mechanisms to block MPF activation in developing oocytes must exist to prevent precocious cell cycle progression prior to oocyte maturation and fertilization. This study sought to determine the developmental consequences of precociously activating MPF in oocytes prior to fertilization. Whereas depletion of Myt1 in Xenopus oocytes causes nuclear envelope breakdown in vitro, we found that depletion of the Myt1 ortholog WEE-1.3 in C. elegans hermaphrodites causes precocious oocyte maturation in vivo. Although such oocytes are ovulated, they are fertilization incompetent. We have also observed novel phenotypes in these precociously maturing oocytes, such as chromosome coalescence, aberrant meiotic spindle organization, and the expression of a meiosis II post-fertilization marker. Furthermore, co-depletion studies of CDK-1 and WEE-1.3 demonstrate that WEE-1.3 is dispensable in the absence of CDK-1, suggesting that CDK-1 is a major target of WEE-1.3 in C. elegans oocytes.
Key words: Oocyte maturation, Meiotic maturation, Myt1, Wee1, Cdk1
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