Developmental mechanisms controlled by Myt 1 kinase

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My laboratory studies how cells reproduce and differentiate during Drosophila development. Defects in these developmental mechanisms are associated with infertility, aging and cancer. Our research focuses on an ancient cell cycle regulatory mechanism, which has been conserved from yeast to humans. We are characterizing the role of a protein called dMyt1 that inhibits certain aspects of cell cycle progression that are controlled by another protein called Cdk1, which functions as a master regulator of cell division. Myt1 seems to function like a Cdk1 "brake", ensuring that important biological processes with many coordinated steps are properly completed, before cells attempt to divide. We are also interested in ways of releasing this Myt1 brake mechanism, so that cells can divide when they are ready. By studying Drosophila myt1 mutants, we have shown that loss of Myt1 activity causes male sterility and is associated with extra, defective cells in certain tissues. We have identified specific sub-cellular defects in myt1 mutant sperm precursor cells that probably account for the male sterility. To functionally characterize this role of dMyt1, we have generated trangenic strains for expressing different forms of the protein during spermatogenesis. By comparing normal and myt1 mutants for clues to Myt1 function, these tools will enable us to design experiments to test proposed models for understanding how Myt1 sub-cellular localization and catalytic activity are regulated. These experiments will clarify how Myt1 activity influences male meiosis and are also expected to reveal features that will help us to understand Myt1 functions at other stages of development.