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Cell

Title:		Pheromone-dependent destruction of the Tec1 transcription factor is required for MAP kinase signaling specificity in yeast
Author(s):		Bao MZ; Schwartz MA; Cantin GT; Yates JR; Madhani HD;
Address:		"Department of Biochemistry and Biophysics, University of California, 600 16th Street, San Francisco, CA 94143, USA"
Journal Title:		Cell
Year:		2004
Volume:		119
Issue:		7
Page Number:		991 - 1000
DOI:		10.1016/j.cell.2004.11.052
ISSN/ISBN:		0092-8674 (Print) 0092-8674 (Linking)
Abstract:		"The yeast MAPK pathways required for mating versus filamentous growth share multiple components yet specify distinct programs. The mating-specific MAPK, Fus3, prevents crosstalk between the two pathways by unknown mechanisms. Here we show that pheromone signaling induces Fus3-dependent degradation of Tec1, the transcription factor specific to the filamentation pathway. Degradation requires Fus3 kinase activity and a MAPK phosphorylation site in Tec1 at threonine 273. Fus3 associates with Tec1 in unstimulated cells, and active Fus3 phosphorylates Tec1 on T273 in vitro. Destruction of Tec1 requires the F box protein Dia2 (Digs-into-agar-2), and Cdc53, the Cullin of SCF (Skp1-Cdc53-F box) ubiquitin ligases. Notably, mutation of the phosphoacceptor site in Tec1, deletion of FUS3, or deletion of DIA2 results in a loss of signaling specificity such that pheromone pathway signaling erroneously activates filamentation pathway gene expression and invasive growth. Signal-induced destruction of a transcription factor for a competing pathway provides a mechanism for signaling specificity"
Keywords:		Amino Acid Sequence Anaphase-Promoting Complex-Cyclosome Cell Cycle Proteins/genetics/metabolism Cullin Proteins/genetics/metabolism DNA-Binding Proteins/genetics/*metabolism F-Box Proteins/genetics/metabolism MAP Kinase Signaling System/*drug effects Mit;
Notes:		"MedlineBao, Marie Z Schwartz, Monica A Cantin, Greg T Yates, John R 3rd Madhani, Hiten D eng R01-GM067880/GM/NIGMS NIH HHS/ R01-GM63670-01/GM/NIGMS NIH HHS/ Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. Research Support, U.S. Gov't, P.H.S. 2004/12/29 Cell. 2004 Dec 29; 119(7):991-1000. doi: 10.1016/j.cell.2004.11.052"