Loss of control of the cell cycle is a defect characteristic of cancer cells. The main hypothesis of this proposal is that the incorporation of myosin II (Myo1p) in the assembly of the actomyosin contractile ring or progression of the cell cycle. Furthermore, we propose that normal adult cell cycle progression is important for the normal regulation of chitin metabolism in these cells. We will also seek to determine if Myo1p function is required for the normal targeting of chitin metabolizing enzymes.
The specific aims of this proposal are: 1) To determine that Myo1p-deficient cells are delayed at G2/M-phase of the cell cycle, to define the specific stage, and to determine the biochemical nature of this delay. 2) To determine the relationship between this putative cell cycle delay and the alterations in chitin metabolism described in Myo1p-deficient cells. 3) To determine the role of Myo1p in the temporal and spatial regulation of chitin synthases 1, 2, and 3. The long-term goal of this study is to define the function(s) of type II myosin in eukaryotic cells. This work will increase our understanding about the integration between specific regulatory processes of the cell cycle and metabolic processes that involve cell wall metabolism and morphogenesis. The information obtained may be employed in the future development of novel approaches for control of fungal growth under laboratory conditions and in clinical settings. The answers to these specific aims will also provide new insights to the function of type II myosin in other eukaryotic cells where similar questions regarding its role in cell growth and morphogenesis are being addressed.
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