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

Ivo Pedruzzi, Niels Bürckert, Pascal Egger, Claudio De Virgilio

Author Affiliations

  1. Ivo Pedruzzi1,
  2. Niels Bürckert1,
  3. Pascal Egger1 and
  4. Claudio De Virgilio*,1
  1. 1 Botanisches Institut der Universität, Hebelstrasse 1, CH‐4056, Basel, Switzerland
  1. *Corresponding author. E-mail: Claudio.DeVirgilio{at}
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The Saccharomyces cerevisiae protein kinase Rim15 was identified previously as a component of the Ras/cAMP pathway acting immediately downstream of cAMP‐dependent protein kinase (cAPK) to control a broad range of adaptations in response to nutrient limitation. Here, we show that the zinc finger protein Gis1 acts as a dosage‐dependent suppressor of the rim15Δ defect in nutrient limitation‐induced transcriptional derepression of SSA3. Loss of Gis1 results in a defect in transcriptional derepression upon nutrient limitation of various genes that are negatively regulated by the Ras/cAMP pathway (e.g. SSA3, HSP12 and HSP26). Tests of epistasis as well as transcriptional analyses of Gis1‐dependent expression indicate that Gis1 acts in this pathway downstream of Rim15 to mediate transcription from the previously identified post‐diauxic shift (PDS) element. Accordingly, deletion of GIS1 partially suppresses, and overexpression of GIS1 exacerbates the growth defect of mutant cells that are compromised for cAPK activity. Moreover, PDS element‐driven expression, which is negatively regulated by the Ras/cAMP pathway and which is induced upon nutrient limitation, is almost entirely dependent on the presence of Gis1.

  • Received February 22, 2000.
  • Revision received April 11, 2000.
  • Accepted April 11, 2000.
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