ArticleCurrent genetics2006
Control of MAPK signaling specificity by a conserved residue in the MEK-binding domain of the yeast scaffold protein Ste5.
Article in Current genetics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- Strain-dependent differences in coordination of yeast signalling networks.The FEBS journal · 2023Article
- Analysis of the thresholds for transcriptional activation by the yeast MAP kinases Fus3 and Kss1.Molecular biology of the cell · 2018Article
- Spatial and temporal signal processing and decision making by MAPK pathways.The Journal of cell biology · 2017Review
- S-sulfhydration of MEK1 leads to PARP-1 activation and DNA damage repair.EMBO reports · 2014Article
- Scaffold proteins: hubs for controlling the flow of cellular information.Science (New York, N.Y.) · 2011Review
- Ultrasensitive responses and specificity in cell signaling.BMC systems biology · 2010Article
- Hog1 mitogen-activated protein kinase (MAPK) interrupts signal transduction between the Kss1 MAPK and the Tec1 transcription factor to maintain pathway specificity.Eukaryotic cell · 2009Article
- Article
- TORC2 plasma membrane localization is essential for cell viability and restricted to a distinct domain.Molecular biology of the cell · 2009Article
- Mapping dynamic protein interactions in MAP kinase signaling using live-cell fluorescence fluctuation spectroscopy and imaging.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Function and regulation in MAPK signaling pathways: lessons learned from the yeast Saccharomyces cerevisiae.Biochimica et biophysica acta · 2007Review
- Mathematical models of specificity in cell signaling.Biophysical journal · 2007Article
- Mechanisms regulating the protein kinases of Saccharomyces cerevisiae.Eukaryotic cell · 2007Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The yeast kinase scaffold Ste5 has been proposed to prevent unwanted cross-talk between the pheromone response pathway and other MAPK cascades. Protein fusion experiments have demonstrated that covalently tethering signaling components to each other or to Ste5 can determine the outcome of signaling. However, these do not fully test the role of scaffolds in signaling specificity, since fusing components precludes differential dissociation of subpopulations. We performed a targeted genetic screen on STE5 and repeatedly identified recessive mutations in a conserved residue, E756, in the Ste7/MEK-binding domain that caused erroneous activation of the filamentation MAPK pathway by pheromone signaling. Mutant cells exhibited a shift in the MAPK activation pattern such that the filamentation MAPK Kss1 was predominately activated in response to pheromone. Velocity sedimentation studies showed that the mutant scaffold was defective in binding to a phosphorylated subpopulation of Ste7. Our data suggest that increased dissociation of activated Ste7 kinase from the mutant scaffold may cause the observed shift in MAPK activation from Fus3 to Kss1 and the resulting loss of specificity. Cross-talk in ste5-E756G cells was due to both increased activation of Kss1 and reduced Fus3-dependent degradation of the filamentation pathway transcription factor Tec1. These studies demonstrate a role for an endogenous scaffold in signaling specificity.
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