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Eukaryotic Cell, December 2006, p. 2147-2160, Vol. 5, No. 12
1535-9778/06/$08.00+0     doi:10.1128/EC.00270-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Pheromone-Induced Degradation of Ste12 Contributes to Signal Attenuation and the Specificity of Developmental Fate{triangledown}

R. Keith Esch,1,{dagger} Yuqi Wang,2 and Beverly Errede1*

Department of Biochemistry and Biophysics, University of North Carolina, Chapel Hill, North Carolina 27599-7260,1 Department of Biology, Saint Louis University, St. Louis, Missouri 63103-20102

Received 25 August 2006/ Accepted 28 September 2006

The Ste12 transcription factor of Saccharomyces cerevisiae regulates transcription programs controlling two different developmental fates. One is differentiation into a mating-competent form that occurs in response to mating pheromone. The other is the transition to a filamentous-growth form that occurs in response to nutrient deprivation. These two distinct roles for Ste12 make it a focus for studies into regulatory mechanisms that impart biological specificity. The transient signal characteristic of mating differentiation led us to test the hypothesis that regulation of Ste12 turnover might contribute to attenuation of the mating-specific transcription program and restrict activation of the filamentation program. We show that prolonged pheromone induction leads to ubiquitin-mediated destabilization and decreased amounts of Ste12. This depletion in pheromone-stimulated cultures is dependent on the mating-pathway-dedicated mitogen-activated protein kinase Fus3 and its target Cdc28 inhibitor, Far1. Attenuation of pheromone-induced mating-specific gene transcription (FUS1) temporally correlates with Ste12 depletion. This attenuation is abrogated in the deletion backgrounds (fus3{Delta} or far1{Delta}) where Ste12 is found to persist. Additionally, pheromone induces haploid invasion and filamentous-like growth instead of mating differentiation when Ste12 levels remain high. These observations indicate that loss of Ste12 reinforces the adaptive response to pheromone and contributes to the curtailing of a filamentation response.

* Corresponding author. Mailing address: Department of Biochemistry and Biophysics, CB 7260 512 ME Jones, University of North Carolina, Chapel Hill, NC 27599-7260. Phone: (919) 966-3628. Fax: (919) 966-4812. E-mail: errede{at}email.unc.edu.

{triangledown} Published ahead of print on 13 October 2006.

{dagger} Present address: Microbial and Molecular Biology Department, RTI International, Research Triangle Park, NC 27709-2194.

Eukaryotic Cell, December 2006, p. 2147-2160, Vol. 5, No. 12
1535-9778/06/$08.00+0     doi:10.1128/EC.00270-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

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  • Yi, S., Sahni, N., Daniels, K. J., Pujol, C., Srikantha, T., Soll, D. R. (2008). The Same Receptor, G Protein, and Mitogen-activated Protein Kinase Pathway Activate Different Downstream Regulators in the Alternative White and Opaque Pheromone Responses of Candida albicans. Mol. Biol. Cell 19: 957-970 [Abstract] [Full Text]  


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