KRH1 and KRH2 are functionally non-redundant in signaling for pseudohyphal differentiation in Saccharomyces cerevisiae.

Diploid cells of Saccharomyces cerevisiae undergo pseudohyphal differentiation in response to nutrient depletion. Although this dimorphic transition occurs due to signals originating from carbon and nitrogen limitation, how these signals are coordinated and integrated is not understood. Results of this study indicate that the pseudohyphal defect of the mep2∆ mutant is overcome upon disruption of KRH2/GPB1 but not KRH1/GPB2. Further, the agar invasion defect observed in a mep2 mutant strain is suppressed only by deleting KRH2 and not KRH1. Thus, the results presented indicate that MEP2 functions by inhibiting KRH2 to trigger filamentation response when glucose becomes limiting. Biochemical data and phenotypic response to glucose replenishment reveal that KRH1 and KRH2 are differentially regulated by glucose and ammonium to induce pseudohyphae formation via the cAMP-PKA pathway. In contrast to the current view, this study clearly demonstrates that, KRH1 and KRH2 are not functionally redundant.