ArticleMolecular and cellular biology2005
Mitogen-activated protein kinases with distinct requirements for Ste5 scaffolding influence signaling specificity in Saccharomyces cerevisiae.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed.
- Phosphoregulation of the novel hemi-arrestin MAPK scaffold Sms1 prevents untimely mating.Nature communications · 2026Article
- Shared and redundant proteins coordinate signal cross-talk between MAPK pathways in yeast.Molecular biology of the cell · 2024Article
- Strain-dependent differences in coordination of yeast signalling networks.The FEBS journal · 2023Article
- New Aspects of Invasive Growth Regulation Identified by Functional Profiling of MAPK Pathway Targets inGenetics · 2020Article
- Osmostress enhances activating phosphorylation of Hog1 MAP kinase by mono-phosphorylated Pbs2 MAP2K.The EMBO journal · 2020Article
- Systematic analysis of F-box proteins reveals a new branch of the yeast mating pathway.The Journal of biological chemistry · 2019Article
- Analysis of the thresholds for transcriptional activation by the yeast MAP kinases Fus3 and Kss1.Molecular biology of the cell · 2018Article
- Modeling evolution of crosstalk in noisy signal transduction networks.Physical review. E · 2018Article
- Nuclear relocation of Kss1 contributes to the specificity of the mating response.Scientific reports · 2017Article
- Signal inhibition by a dynamically regulated pool of monophosphorylated MAPK.Molecular biology of the cell · 2015Article
- The Dictyostelium MAPK ERK1 is phosphorylated in a secondary response to early developmental signaling.Cellular signalling · 2015Article
- Combined computational and experimental analysis reveals mitogen-activated protein kinase-mediated feedback phosphorylation as a mechanism for signaling specificity.Molecular biology of the cell · 2012Article
- Response to hyperosmotic stress.Genetics · 2012Review
- Conformational control of the Ste5 scaffold protein insulates against MAP kinase misactivation.Science (New York, N.Y.) · 2012Article
- The regulation of filamentous growth in yeast.Genetics · 2012Review
- How scaffolds shape MAPK signaling: what we know and opportunities for systems approaches.Frontiers in physiology · 2012Article
- Scaffold proteins: hubs for controlling the flow of cellular information.Science (New York, N.Y.) · 2011Review
- Design principles and specificity in biological networks with cross activation.Physical biology · 2011Article
- MAPKs in development: insights from Dictyostelium signaling pathways.Biomolecular concepts · 2011Article
- Ultrasensitive responses and specificity in cell signaling.BMC systems biology · 2010Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Scaffold proteins are believed to enhance specificity in cell signaling when different pathways share common components. The prototype scaffold Ste5 binds to multiple components of the Saccharomyces cerevisiae mating pheromone response pathway, thereby conducting the mating signal to the Fus3 mitogen-activated protein kinase (MAPK). Some of the kinases that Ste5 binds to, however, are also shared with other pathways. Thus, it has been presumed that Ste5 prevents its bound kinases from transgressing into other pathways and protects them from intrusions from those pathways. Here we found that Fus3MAPK required Ste5 scaffolding to receive legitimate signals from the mating pathway as well as misdirected signals leaking from other pathways. Furthermore, increasing the cellular concentration of active Ste5 enhanced the channeling of inappropriate stimuli to Fus3. This aberrant signal crossover resulted in the erroneous induction of cell cycle arrest and mating. In contrast to Fus3, the Kss1 MAPK did not require Ste5 scaffolding to receive either authentic or leaking signals. Furthermore, the Ste11 kinase, once activated via Ste5, was able to signal to Kss1 independently of Ste5 scaffolding. These results argue that Ste5 does not act as a barrier that actively prevents signal crossover to Fus3 and that Ste5 may not effectively sequester its activated kinases away from other pathways. Rather, we suggest that specificity in this network is promoted by the selective activation of Ste5 and the distinct requirements of the MAPKs for Ste5 scaffolding.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.