FAR1 is required for posttranscriptional regulation of CLN2 gene expression in response to mating pheromone.

Abstract

heterotrimeric G protein-coupled cell surface receptor (encoded by STE3 or STE2). Many of the other components of this transduction pathway are known. The induction of mating pheromone-specific genes occurs through the action of the STE12 gene product as a consequence of its binding to a pheromone-specific transcription-activating sequence known as the pheromone response element (11,14). Several of these pheromone-specific genes are known to be involved in the mating process. In contrast, the mechanism by which the same pathway results in G1-specific cell cycle arrest is not understood. Although STE12 function has been implicated in this arrest, the nature of its involvement is not known (10).Cell cycle progression in budding yeasts is known to require the activity of the CDC28 gene product (20,34,35), a serine/threonine protein kinase of the Cdk (cyclin-dependent kinase) family, which includes the Cdc2 protein kinase (reviewed by Pines and Hunter [32]). The function of the CDC28 gene product is essential for passage through the G1/S and G2/M transitions. Its role at each of these transitions is performed in conjunction with those of distinct families of cyclin proteins, the G2/M function requiring B-type cyclins encoded by the CLB genes (16,40) and the role during G1 phase requiring the G1 cyclins encoded by the CLN genes. The CLN gene family consists of three genes, CLN1, CLN2, and CLN3, which perform an overlapping function that is essential for progression through G1 phase (5,18,27,36

G1 cyclins CLN1 and CLN2 repress the mating factor response pathway at Start in the yeast cell cycle.

“…McKinney and F. Cross, unpubl. ) but can also interfere, probably at the post-transcriptional level, with the functioning of Clnl, as has been suggested earlier by others (Valdivieso et al 1993).…”

“…In contrast, induction of FUS1-lacZ by mating factor was greatly reduced in cells overexpressing CLN2. Farlp is thought to act negatively on Cln function (Chang and Herskowitz 1990;Valdivieso et al 1993;Peter et al 1993;; therefore, disruption of the FAR1 gene might further stimulate Cln-Cdc28p activity. Consistent with this idea, FUS1 signaling in f a r l -strains overexpressing CLN1 was found to be lower than in FAR1 + strains.…”

High Functional Overlap Between MluI Cell-Cycle Box Binding Factor and Swi4/6 Cell-Cycle Box Binding Factor in the G1/S Transcriptional Program in Saccharomyces cerevisiae

“…To construct the normally inviable double mutant strain, we made use of the observation of Koch et al (1993) that mbp1 swi4 mutants were viable when CLN2 was placed under control of a constitutive promoter. We observed reasonably efficient rescue of viable mbp1 swi4 mutant strains by inclusion of an integrated construct containing CLN2 under the control of the CLN3 promoter, P CLN3 -CLN2 (Valdivieso et al 1993;Levine et al 1996).…”

CLB5 and CLB6, a new pair of B cyclins involved in DNA replication in Saccharomyces cerevisiae.

“…7). Thus, unlike the case for Clnl and Cln2 (Valdivieso et al 1993), pheromones might not be able to regulate Clb5 activity at a post-transcriptional level.…”

“…Cyclin types are not only distinguished by the range of cell cycle events that they affect but also by the different forms of regulation imposed on them. Pheromonal control, for example, may be exerted directly on Cln cyclin activity via the Farl protein and not directly on other cyclin types such as Clb5 (Chang and Herskowitz 1990;Valdivieso et al 1993). This could explain why expression of CLB5 from the GAL promoter allows cells to escape pheromone-induced G1 arrest.…”