We designed a screen to isolate temperature sensitive lethal mutants that undergo START in the presence of pheromone and has a normal transcriptional response to pheromone. The isolated mutants belong to 4 complementation groups ARE1,2,3,4 (alpha-factor resistant essential). At restrictive temperature in the presence of pheromone they bud and replicate their DNA. After two hours the transcriptional activity of the pathway declines as measured by the level of the FUS1 mRNA. This phenotype indicates that the mutants are defective in maintaining the integrity of the signaling pathway. Since the mutants are not specifically defective in cell cycle arrest in response to pheromone, we asked at which level they affect the signaling pathway. We took the advantage of inducible activating alleles of components of the pathway. Our results show that the mutants affect different steps in the signaling cascade. The isolation of SAR1-20, a dominant second site suppressor of are1-1 showed that the vegetative growth and the pheromone signal transduction functions are separable of the ARE1 gene. We obtained complementing genomic DNA fragments for are1,2,3,4 and SAR1-20. ARE3 maps to the ORF of the CCL1 gene which has a role in general transcription. BLAST searches of ARE1 and ARE4 ORF did not show high homology to known genes.