UC Santa Cruz

The adult human body is made up of trillions of cells and yet began as just one. This could not be possible without careful coordination of cell growth and cell division. The molecular mechanisms that drive and control cell growth as well as its coordination with the cell cycle remain poorly understood. Cell size is the outcome of cell growth. Thus, a decoupling of growth and division would result in cells of increasingly heterogenous sizes. Interestingly, the severity of a cancer is often correlated with increasingly heterogenous size of cells within a tissue. Furthermore, genes that are thought to play important roles in cell growth are often dysregulated in a variety of cancers. This suggests that the misregulation of mechanisms that control cell growth and cell size plays a role in cancer cell development. How cell growth influences cell cycle progression to control cell size is perhaps best understood in budding yeast where key cell cycle transitions are delayed until sufficient growth has occurred. It had been long believed that the predominant cell size checkpoint in budding yeast occurred at cell cycle entry. Recent work, however, suggests that bud growth strongly influences cell cycle progression in mitosis. In this thesis, I present evidence to support a model in which cells influence the extent and duration of bud growth by controlling mitotic exit, a cell cycle transition that seizes bud growth and finalizes daughter cell size.