Mating pheromone inhibits cell division in the absence of FAR1 and FUS3. V. Cherkasova and E.A. Elion, Harvard Medical School, 240 Longwood Ave. Boston, MA 02115, 617-432-3814. To date, Fus3, a MAP kinase, and Far1, a protein that inhibits G1 cyclin/Cdc28 complexes, are the only known mediators of G1 arrest during mating in S. cerevisiae. We present evidence that argues that G1 arrest involves additional regulatory events distinct from Fus3 and Far1. First, *alpha* factor sensitivity can be restored to fus3*delta* and far1*delta* null mutants by increasing the level of signaling through a variety of means. Second, this suppression is associated with accumulation of unbudded cells, and restored inhibition of CLN1,2 transcription, Cdc28 activity, and DNA synthesis. Third, suppression requires known components of the mating signal transduction cascade, including Kss1 which was not known to have a distinct role in G1 arrest. We find that pheromone-dependent inhibition of growth does not always correlate with a coordinate inhibition of budding, DNA replication and Cdc28 activity. This suggests the existence of separate branches for inhibition of budding and DNA replication that are independent of total Cdc28 inhibition. To identify new regulators of G1 arrest that are functionally redundant with Far1, we performed a selection for *alpha* factor resistant mutants that are signaling competent using an a factor sensitive far1*delta* strain. The recessive mutations define 3 putative regulators that are not complemented by any of the known signaling genes nor by FAR3.