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Myb-related Schizosaccharomyces pombe cdc5p is structurally and functionally conserved in eukaryotes
R Ohi1, A Feoktistova, S McCann
1Department of Cell Biology, School of Medicine, Vanderbilt University, Nashville, Tennessee 37232, USA.
Molecular and Cellular Biology
|June 25, 1998
Summary
Cdc5 proteins, essential for cell cycle G2/M progression, are conserved across species. Myb repeats are crucial for function, but their structure differs from c-Myb, suggesting a novel regulatory pathway.
Area of Science:
- Cell Biology
- Molecular Biology
- Genetics
Background:
- The Myb-related protein Cdc5p in Schizosaccharomyces pombe is vital for G2/M cell cycle progression.
- Understanding the evolutionary conservation of Cdc5 is key to elucidating its fundamental roles.
Purpose of the Study:
- To investigate the structural and functional conservation of Cdc5 proteins across diverse species.
- To explore the role of Myb repeats in Cdc5 function and identify potential novel regulatory pathways.
Main Methods:
- Isolation of Cdc5-related genes and cDNAs from Saccharomyces cerevisiae, Caenorhabditis elegans, Drosophila melanogaster, and Homo sapiens.
- Functional complementation assays using S. pombe cdc5-120 mutant.
- Site-directed mutagenesis of S. cerevisiae CEF1 (Cef1p) Myb repeats.
- Analysis of transcriptional activation of G2/M-regulated genes.
Main Results:
- Cdc5 cDNAs from humans and flies functionally complemented the S. pombe cdc5-120 mutant.
- S. cerevisiae CEF1 is essential for G2/M progression.
- Myb repeats of Cdc5p and Cef1p are important for in vivo function, though structural requirements differ from c-Myb.
- Multiple mutations in Cef1p's Myb repeats were needed for inactivation, and Cef1p does not activate SWI5 transcription.
Conclusions:
- Cdc5 family members are functionally conserved across evolution, playing essential roles in G2/M progression.
- The Myb repeats of Cdc5 proteins are critical for function, but exhibit distinct structural-functional relationships compared to c-Myb.
- Cdc5 proteins likely operate through a novel pathway to regulate the G2/M transition, independent of direct transcriptional activation of certain G2/M genes.