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Eukaryotic Cell, June 2004, p. 610-619, Vol. 3, No. 3
1535-9778/04/$08.00+0     DOI: 10.1128/EC.3.3.610-619.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Suppressors of an Adenylate Cyclase Deletion in the Fission Yeast Schizosaccharomyces pombe

Jeffrey Stiefel,1,{dagger} Lili Wang,1 David A. Kelly,1 Rozmin T. K. Janoo,1,{ddagger} Jeffrey Seitz,1 Simon K. Whitehall,2 and Charles S. Hoffman1*

Biology Department, Boston College, Chestnut Hill, Massachusetts 02467,1 School of Cell and Molecular Biosciences, University of Newcastle upon Tyne, Newcastle NE2 4HH, United Kingdom2

Received 16 March 2004/ Accepted 2 April 2004

Schizosaccharomyces pombe utilizes two opposing signaling pathways to sense and respond to its nutritional environment. Glucose detection triggers a cyclic AMP signal to activate protein kinase A (PKA), while glucose or nitrogen starvation activates the Spc1/Sty1 stress-activated protein kinase (SAPK). One process controlled by these pathways is fbp1+ transcription, which is glucose repressed. In this study, we isolated strains carrying mutations that reduce high-level fbp1+ transcription conferred by the loss of adenylate cyclase (git2{Delta}), including both wis1– (SAPK kinase) and spc1– (SAPK) mutants. While characterizing the git2{Delta} suppressor strains, we found that the git2{Delta} parental strains are KCl sensitive, though not osmotically sensitive. Of 102 git2{Delta} suppressor strains, 17 strains display KCl-resistant growth and comprise a single linkage group, carrying mutations in the cgs1+ PKA regulatory subunit gene. Surprisingly, some of these mutants are mostly wild type for mating and stationary-phase viability, unlike the previously characterized cgs1-1 mutant, while showing a significant defect in fbp1-lacZ expression. Thus, certain cgs1– mutant alleles dramatically affect some PKA-regulated processes while having little effect on others. We demonstrate that the PKA and SAPK pathways regulate both cgs1+ and pka1+ transcription, providing a mechanism for cross talk between these two antagonistically acting pathways and feedback regulation of the PKA pathway. Finally, strains defective in both the PKA and SAPK pathways display transcriptional regulation of cgs1+ and pka1+, suggesting the presence of a third glucose-responsive signaling pathway.

* Corresponding author. Mailing address: Biology Department, Boston College, 140 Commonwealth Ave., Higgins Hall 401B, Chestnut Hill, MA 02467. Phone: (617) 552-2779. Fax: (617) 552-2011. E-mail: hoffmacs{at}bc.edu.

{dagger} Present address: Office of the Assistant Secretary of the Army, Pentagon, Washington, D.C. 20310-0103.

{ddagger} Present address: Cancer Control Research BC Cancer Agency, Vancouver, British Columbia V5Z 4C2, Canada.

Eukaryotic Cell, June 2004, p. 610-619, Vol. 3, No. 3
1535-9778/04/$08.00+0     DOI: 10.1128/EC.3.3.610-619.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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