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Defects in Protein Glycosylation Cause SHO1-Dependent Activation of a STE12 Signaling Pathway in Yeast
Paul J. Cullena, Janet Schultza, Joe Horeckab, Brian J. Stevensona, Yoshifumi Jigamib, and George F. Sprague, Jr.aa Institute of Molecular Biology, University of Oregon, Eugene, Oregon 97403-1229
b National Institute of Bioscience and Human Technology, Agency of Industrial Science and Technology, Tsukuba, Ibaraki 305-8566, Japan
Corresponding author: George F. Sprague, Jr., Institute of Molecular Biology, University of Oregon, Eugene, OR 97403-1229., gsprague{at}molbio.uoregon.edu (E-mail)
Communicating editor: A. P. MITCHELL
Ste20/Ste50
Ste11
Ste7
Kss1
Ste12 pathway is responsible for activation of FUS1 transcription in these mutants. Because loss of pheromone response pathway components leads to a synthetic growth defect in mannose utilization/protein glycosylation mutants, we suggest that the Sho1
Ste12 pathway contributes to maintenance of cell wall integrity in vegetative cells.
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