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Dev Biol. 1999 Feb 1;206(1):15-32.

RNA-Mediated interference of a cdc25 homolog in Caenorhabditis elegans results in defects in the embryonic cortical membrane, meiosis, and mitosis.

Author information

1
Developmental Signal Transduction Group, Gene Regulation and Chromosome Biology Laboratory, ABL-Basic Research Program, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, Maryland, 21702, USA.

Abstract

The CDC25 dual-specificity phosphatase family has been shown to play a key role in cell cycle regulation. The phosphatase activity of CDC25 drives the cell cycle by removing inhibitory phosphates from cyclin-dependent kinase/cyclin complexes. Although the regulation of CDC25 phosphatase activity has been elucidated both biochemically and genetically in other systems, the role of this enzyme during development is not well understood. To examine the expression pattern and function of CDC25 in Caenorhabditis elegans, we characterized a cdc25 homolog, cdc-25.1, during early embryonic development. The CDC-25.1 protein localizes to oocytes, embryonic nuclei, and embryonic cortical membranes. When the expression of CDC-25.1 was disrupted by RNA-mediated interference, the anterior cortical membrane of fertilized eggs became very fluid during meiosis and subsequent mitotic cell cycles. Mispositioning of the meiotic spindle, defects in polar body extrusion and chromosome segregation, and abnormal cleavage furrows were also observed. We conclude that CDC-25.1 is required for a very early developmental process-the proper completion of meiosis prior to embryogenesis.

PMID:
9918692
DOI:
10.1006/dbio.1998.9135
[Indexed for MEDLINE]
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