Saccharomyces cerevisiae Ras/cAMP pathway controls post-diauxic shift element-dependent transcription through the zinc finger protein Gis1

The Saccharomyces cerevisiae protein kinase Rim15 was identified previously as a component of the Ras/cAMP pathway acting immediately downstream of cA MP-dependent protein kinase (cAPK) to control a broad range of adaptations in response to nutrient limitation. Here, we show that the zinc finger prot ein Gis1 acts as a dosage-dependent suppressor of the vim15 Delta defect in nutrient limitation-induced transcriptional derepression of SSA3, Loss of Gis1 results in a defect in transcriptional derepression upon nutrient limi tation of various genes that are negatively regulated by the Ras/cAMP pathw ay (e.g, SSA3, HSP12 and HSP26). Tests of epistasis as well as transcriptio nal analyses of Gis1-dependent expression indicate that Gis1 acts in this p athway downstream of Rim15 to mediate transcription from the previously ide ntified post-diauxic shift (PDS) element. Accordingly, deletion of GIS1 par tially suppresses, and overexpression of GIS1 exacerbates the growth defect of mutant cells that are compromised for cAPK activity. Moreover, PDS elem ent-driven expression, which is negatively regulated by the Ras/cAMP pathwa y and which is induced upon nutrient limitation, is almost entirely depende nt on the presence of Gis1.