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 G2. 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 for G1(S progression, 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. Cells also compensate by shortening G2 when G1 is elongated by overexpression of dacapo, a specific inhibitor of Cyclin E. In this situation, accumulation of String is observed and thought to be involved in the shortening of G2. When G2 is elongated by overexpression of dwee1, a specific inhibitor of the CdK1 activity, cells compensate by upregulating Cyclin E, which results in the shortening of G1. dE2F1, a transcription factor that can drive expression of cyclin E and string, is a common player in these two situations. Compensation involves upregulation of E2F1 protein levels and activity, and this may be responsible for upregulating string levels in a G1-elongated cycle and cyclin E levels in a G2-elongated cycle. These results indicate that cells can compensate not only for the truncation but also for the elongation of phases, and suggest that coordination of G1(S and G2(M progression is mediated by a common regulator, E2F1.