G1-G2 cell cycle compensation. T. Reis , B. Edgar. Basic Sciences, Fred Hutchinson CRC, Seattle, WA.

   During early stages of Drosophila development cell number increases exponentially in a short period of time. In larval wing discs cell division is coupled with growth and is characterized by a G1-S-G2-M cell cycle. String is the limiting factor for G2-M passage of the cell cycle. Overexpression of string shortens the G2 phase of the cycle. Interestingly, this does not result in a shorter cycle in the wing. Cells compensate for the accelerated passage through G2 by spending more time in G1, resulting in cell cycle lengths comparable to wild-type. Similarly, overexpression of cyclin E, the limiting factor that drives G1 into S phase, results in cells with an abbreviated G1 phase, as expected, but extended S phase, resulting again in a cell cycle length similar to wild-type. These results suggest a new mechanism of cell cycle control that enables cells to cycle at normal rates even when one of the phases is accelerated. A similar compensatory mechanism has been previously observed in other systems such as yeast and mammalian tissue culture. Preliminary results indicate a possible compensatory mechanism when G1 is elongated by overexpression of dacapo, a specific inhibitor of Cyclin E. Together with the previous results this indicates that cells can compensate not only for the elongation but also for the truncation of phases. The aim of this work is to understand the mechanism behind this compensatory effect. The question of how cells measure their rates of division and growth at different cell cycle phases and how, when and why they use this mechanism will also be addressed.