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The Role of Pangu and Endos on Embryonic Mitosis Through the Regulation of Cdk1/cdc2-cyclin B Activity in Drosophila Melanogaster

Undergraduate #20
Discipline: Biological Sciences
Subcategory: Cancer Research

Carlos A. Betancourt - California State University, San Marcos
Co-Author(s): Helene Rangone and David M. Glover, Cambridge University, Cambridge, United Kingdom



In addition to and synergizing Cdk1/cdc2-Cyclin B activity, the Polo and Greatwall kinases are important protein kinases for the regulation of mitosis. In particular, Greatwall promotes Cdk1/ cdc2-Cyclin B activity by inhibiting its opposing phosphatase PP2A. This is achieved by the phosphorylation of the substrate of Greatwall, Endos, which once phosphorylated directly inhibits PP2A. Moreover greatwall has been found to genetically interact with pangu, the catalytic subunit of a wider complex made of two other regulatory subunits, Plutonium and Giant nuclei. These genes are needed to control the S-M cycles of Drosophila melanogaster embryogenesis by enhancing Cyclin B translation and cdk1/cdc2-Cyclin B activity, which is portrayed by the lethality of the embryos resulting from females mutant for any of the pangu complex genes. Generations of mutant flies were selectively bred in order to investigate whether down-regulating the activity of PP2A (which counterbalances cdk1) with PP2A mutants or by increasing Endos dosage would rescue the mitotic failure of pangu mutant embryos. Three separate experiments resulted in variability of the rescue level. The results suggest that although Pan Gu and Endos cooperatively control the level of active cdk1/Cyclin B activity in embryogenesis, this is not the only pathway in which they interact.

Funder Acknowledgement(s): MHIRT

Faculty Advisor: Angelica Rocha,

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This material is based upon work supported by the National Science Foundation (NSF) under Grant No. DUE-1930047. Any opinions, findings, interpretations, conclusions or recommendations expressed in this material are those of its authors and do not represent the views of the AAAS Board of Directors, the Council of AAAS, AAAS’ membership or the National Science Foundation.

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