Activation of the yeast pheromone response pathway has three key
effects: transcription induction of mating specific genes; G1 arrest;
and shmoo formation. FAR3 is one of several genes required for
G1 arrest. However Far3p does not appear to participate in any of the
previously characterized mechanisms by which pheromone response gives
rise to G1 arrest. In an effort to learn about the mechanism by which
Far3p acts, we have carried out two-hybrid screens. We have identified
nine putative Far3p interactors. Three of these were initially
selected for further characterization. As is observed for far3
mutants, null mutants of FRG1, 2, or 3
(FAR3 interactor Required for G1 arrest)
recover from pheromone-induced G1 arrest more rapidly than the wild
type. Over-expression studies show that high levels of Far3p or Frg2p
can restore G1 arrest in far3, frg1, frg2, or
frg3 mutants. The effect of over-expressing Frg1p or Frg3p has
not yet been examined. Conversely, over-expressing truncated versions
of Frg1p or Frg3p causes a G1 arrest defect in the
wild-type. Truncated versions of Far3p or Frg2p have not yet been
tested. Subcellular fractionation of Far3p, Frg1p, and Frg2p reveals
that all three proteins are present in the same fraction. Localization
of Frg3p is underway. In toto, these data support the notion that
Far3p and its interactors function together to regulate G1 arrest.
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