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Eukaryotic Cell, April 2009, p. 606-616, Vol. 8, No. 4
1535-9778/09/$08.00+0     doi:10.1128/EC.00005-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Hog1 Mitogen-Activated Protein Kinase (MAPK) Interrupts Signal Transduction between the Kss1 MAPK and the Tec1 Transcription Factor To Maintain Pathway Specificity{triangledown} ,{dagger}

Teresa R. Shock,1 James Thompson,2 John R. Yates III,2 and Hiten D. Madhani1*

Department of Biochemistry and Biophysics, University of California at San Francisco, 600 16th St., San Francisco, California 94158,1 The Scripps Research Institute, 10666 N. Torrey Pines Rd., La Jolla, California 920372

Received 4 January 2009/ Accepted 1 February 2009

In Saccharomyces cerevisiae, the mating, filamentous growth (FG), and high-osmolarity glycerol (HOG) mitogen-activated protein kinase (MAPK) signaling pathways share components and yet mediate distinct responses to different extracellular signals. Cross talk is suppressed between the mating and FG pathways because mating signaling induces the destruction of the FG transcription factor Tec1. We show here that HOG pathway activation results in phosphorylation of the FG MAPK, Kss1, and the MAPKK, Ste7. However, FG transcription is not activated because HOG signaling prevents the activation of Tec1. In contrast to the mating pathway, we find that the mechanism involves the inhibition of DNA binding by Tec1 rather than its destruction. We also find that nuclear accumulation of Tec1 is not affected by HOG signaling. Inhibition by Hog1 is apparently indirect since it does not require any of the consensus S/TP MAPK phosphorylation sites on Tec1, its DNA-binding partner Ste12, or the associated regulators Dig1 or Dig2. It also does not require the consensus MAPK sites of the Ste11 activator Ste50, in contrast to a recent proposal for a role for negative feedback in specificity. Our results demonstrate that HOG signaling interrupts the FG pathway signal transduction between the phosphorylation of Kss1 and the activation of DNA binding by Tec1.

* Corresponding author. Mailing address: Department of Biochemistry and Biophysics, University of California at San Francisco, 600 16th St., San Francisco, CA 94158. Phone: (415) 514-0594. Fax: (415) 502-4315. E-mail: hitenmadhani{at}gmail.com

{triangledown} Published ahead of print on 13 February 2009.

{dagger} Supplemental material for this article may be found at http://ec.asm.org/.

Eukaryotic Cell, April 2009, p. 606-616, Vol. 8, No. 4
1535-9778/09/$08.00+0     doi:10.1128/EC.00005-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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