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Molecular and Cellular Biology, June 2002, p. 3994-4000, Vol. 22, No. 12
0270-7306/02/$04.00+0     DOI: 10.1128/MCB.22.12.3994-4000.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Snf1 Protein Kinase and the Repressors Nrg1 and Nrg2 Regulate FLO11, Haploid Invasive Growth, and Diploid Pseudohyphal Differentiation

Sergei Kuchin,1 Valmik K. Vyas,2 and Marian Carlson1,2*

Departments of Genetics and Development and Microbiology,1 Integrated Program in Cellular, Molecular, and Biophysical Studies, Columbia University, New York, New York 100322

Received 28 January 2002/ Returned for modification 13 March 2002/ Accepted 22 March 2002

The Snf1 protein kinase of Saccharomyces cerevisiae is important for many cellular responses to glucose limitation, including haploid invasive growth. We show here that Snf1 regulates transcription of FLO11, which encodes a cell surface glycoprotein required for invasive growth. We further show that Nrg1 and Nrg2, two repressor proteins that interact with Snf1, function as negative regulators of invasive growth and as repressors of FLO11. We also examined the role of Snf1, Nrg1, and Nrg2 in two other Flo11-dependent processes. Mutations affected the initiation of biofilm formation, which is glucose sensitive, but also affected diploid pseudohyphal differentiation, thereby unexpectedly implicating Snf1 in a response to nitrogen limitation. Deletion of the NRG1 and NRG2 genes suppressed the defects of a snf1 mutant in all of these processes. These findings suggest a model in which the Snf1 kinase positively regulates Flo11-dependent developmental events by antagonizing Nrg-mediated repression of the FLO11 gene.


* Corresponding author. Mailing address: 701 W. 168th St., HSC922, New York, NY 10032. Phone: (212) 305-6314. Fax: (212) 305-1741. E-mail: mbc1{at}columbia.edu.


Molecular and Cellular Biology, June 2002, p. 3994-4000, Vol. 22, No. 12
0022-538X/02/$04.00+0     DOI: 10.1128/MCB.22.12.3994-4000.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.




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