SOK2 MAY REGULATE CYCLIC-AMP-DEPENDENT PROTEIN KINASE-STIMULATED GROWTH AND PSEUDOHYPHAL DEVELOPMENT BY REPRESSING TRANSCRIPTION

Yeast cyclic AMP (cAMP)-dependent protein kinase (PKA) activity is ess ential for growth and cell cycle progression. Dependence on PKA functi on can be partially relieved by overexpression of a gene, SOK2, whose product has significant homology with several fungal transcription fac tors (StuA from Aspergillus nidulans and Phd1 from Saccharomyces cerev isiae) that are associated with cellular differentiation and developme nt. Deletion of SOK2 is not lethal but exacerbates the growth defect o f strains compromised for PKA activity. Alterations in Sok2 protein pr oduction also affect the expression of genes involved in several other PKA-regulated processes, including glycogen accumulation (GAC1) and h eat shock resistance (SSA3). These results suggest SOK2 plays a genera l regulatory role in the PKA signal transduction pathway. Expression o f the PKA catalytic subunit genes is unaltered by deletion or overexpr ession of SOX2. Because homozygous sok2/sok2 diploid strains form pseu dohyphae at an accelerated rate, the Sok2 protein may inhibit the swit ch from unicellular to filamentous growth, a process that is dependent on cAMP. Thus, the product of SOK2 may act downstream of PKA to regul ate the expression of genes important in growth and development.