Yeast Genetics and Molecular Biology 2002
University of Wisconsin
Madison, Wisconsin USA
July 30 - August 4, 2002


Name: Bardwell, Lee
Mailing Address: Developmental & Cell Biology, Univ. of California, Irvine, 5207 McGaugh Hall, Irvine, CA 92697-2300, USA
Email Address: bardwell@uci.edu
Phone & FAX numbers: (949) 824-6902 & (949) 824-6908
URL: http://darwin.bio.uci.edu/~bardwell

Abstract #1


Session Title: Signaling Networks
Session Time: Tuesday, July 30 -- 7:00PM - 8:30PM
Presentation: Platform
Topic: Cell Biology

Specificity of MAP kinase signaling in yeast differentiation.
Lee Bardwell, Walid Sabbagh, Laura Flatauer
Developmental & Cell Biology, Univ. of California, Irvine, 5207 McGaugh Hall, Irvine, CA 92697-2300, USA

Often, the transmission of different upstream signals involves common components, yet elicits distinct (and appropriate) outcomes. How specificity from signal to cellular response is maintained in such cases is not well understood. In haploid cells of the yeast S. cerevisiae, two distinct developmental options - mating and filamentous invasive growth - are both regulated by the same mitogen-activated protein kinase (MAPK) cascade, containing the MAPK kinase Ste7 and its target MAPKs Kss1 and Fus3. Despite this overlap, exposure of cells to mating pheromone does not result in the hyperactivation of filamentation genes. Our recent studies indicate that signal identity in this system is encoded in the magnitude and duration of MAPK activation, and not by competition for pathway-specific components. Hence, the yeast model bears a much closer resemblance to the paradigm of proliferation vs. differentiation in mammalian cells, as exemplified by the PC12 system, than was previously appreciated. MAPK activation during mating is transient because one of the MAPKs (Fus3) initiates a negative feedback circuit that downregulates the phosphorylation of both MAPKs. Our latest findings regarding the molecular mechanism of this feedback will be presented.


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