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Full Abstracts – CELL CYCLE AND CELL DEATH
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Identification of factors that cooperate with rbf1 mutations.
Nam-Sung Moon, Kate Krivy, Mary-Rose Bradley-Gill. Department of Biology,
Developmental Biology Research Initiative, McGill University, Montreal, Quebec H3A 1B1, Canada.
Mutations of rbf1, the Drosophila homolog of the Rb tumor suppressor gene, generate defects in cell death and cell cycle control during development. In
the Drosophila eye, RBF1 protects cells entering the Morphogenetic Furrow (MF) from Hid-dependent cell death and cooperates with Dacapo (DAP) to
promote cell cycle exit of differentiating photoreceptors. Interestingly, the EGFR/Ras pathway regulates both Hid and DAP, suggesting that extensive
crosstalk exists between RBF1 and the EGFR/Ras pathway. In an effort to identify downstream effectors of the EGFR/Ras pathway that participate in this
crosstalk, we discovered that Capicua (Cic) regulates both survival and proliferation of rbf1 mutant cells. Cic is a transcription factor whose activity is post-
transcriptionally regulated by the EGFR/Ras pathway, and has been shown to function in restricting proliferation. Immunostaining of imaginal discs revealed
that cic rbf1 double mutant cells display a decreased level of cell death and bypass developmentally controlled cell cycle arrest. We will discuss our effort to
investigate the molecular mechanism underlying this genetic interaction.