When budding yeast growing on a poor carbon source are shifted to glucose they undergo a transient G1 phase lag associated with an increase in the minimal cell size at Start. The lag depends upon the RAS/cAMP pathway and is mimicked by increasing the level of cAMP. To understand the mechanism by which this signal is transduced to the cell cycle machinery we have evaluated the role of G1 cyclins in the response. Using synchronous populations of small G1 daughter cells prepared by centrifugal elutriation we have confirmed that this effect is mediated primarily through regulation of CLN1 and to a lesser extent CLN2. Inactivation of both genes abrogates the G1 delay. This is not due to the increased cell size of these mutants, since constitutive low level expression of CLN2 restores a small minimal cell size without restoring the lag. However, CLN2 expressed in the same manner in otherwise wild type cells fails to abrogate the G1 lag. These results suggest that the effect is exerted at the level of CLN transcription. RNA analysis showed that CLN1 transcription is dramatically repressed in response to glucose while expression of CLN2 is only modestly delayed. We are evaluating whether this difference results from differences in the targets for SBF in the CLN1 and CLN2 promoters or whether other CLN1 promoter elements are targets for negative regulation in response to glucose.