The duration of mitosis and daughter cell size are modulated by nutrients in budding yeast
Abstract
It is virtually impossible to think of cell division without thinking of cellular growth. If cells would divide without growing an adult organism would be as big as the cells that it originated from. Growth must, therefore, be coupled with cellular division with a precision so great that all cells of a given tissue maintain, as we know, remarkably little variation in size.
Maintaining cell size homeostasis is critical for life. Not only is cellular hypertrophy known as an adaptive mechanism in response to metabolic demand, loss of size control is also commonly associated with malignancy.
Coordination of cell size and division is achieved via cell size checkpoints which ensure that a cell has grown enough before it progresses through the cell cycle. Cell size checkpoints are best known in yeast where a sole checkpoint is believed to regulate cell size. Such checkpoint has been described to occur at the G1/S transition. In this thesis I revisit old concepts at the light of new techniques and present results that support the hypothesis that significant cell size regulation occurs during mitosis. In addition I will provide evidence that suggest that mitotic cell size regulation is achieved through coordination of the phosphatase PP2A Rts1 and the kinase Gin4. Cooperatively they control Swe1 activity in response to nutrients, allowing for nutrient modulation of cell size.