ArticleThe FEBS journal2023
Strain-dependent differences in coordination of yeast signalling networks.
Article in The FEBS journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- Surprising regulatory plasticity for the conserved HOG pathway in diversebioRxiv : the preprint server for biology · 2025Article
- Peroxiredoxin Tsa1 Regulates the Activity of Trehalose Metabolism-Related Enzymes During Wine Yeast Biomass Propagation.Microbial biotechnology · 2025Article
- Evaluating cellular roles and phenotypes associated with trehalose degradation genes in Saccharomyces cerevisiae.G3 (Bethesda, Md.) · 2024Article
- TheInternational journal of molecular sciences · 2023Article
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3 authors.
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Abstract
The yeast mitogen-activated protein kinase pathways serve as a model system for understanding how network interactions affect the way in which cells coordinate the response to multiple signals. We have quantitatively compared two yeast strain backgrounds YPH499 and ∑1278b (both of which have previously been used to study these pathways) and found several important differences in how they coordinate the interaction between the high osmolarity glycerol (HOG) and mating pathways. In the ∑1278b background, in response to simultaneous stimulus, mating pathway activation is dampened and delayed in a dose-dependent manner. In the YPH499 background, only dampening is dose-dependent. Furthermore, leakage from the HOG pathway into the mating pathway (crosstalk) occurs during osmostress alone in the ∑1278b background only. The mitogen-activated protein kinase Hog1p suppresses crosstalk late in an induction time course in both strains but does not affect the early crosstalk seen in the ∑1278b background. Finally, the kinase Rck2p plays a greater role suppressing late crosstalk in the ∑1278b background than in the YPH499 background. Our results demonstrate that comparisons between laboratory yeast strains provide an important resource for understanding how signalling network interactions are tuned by genetic variation without significant alteration to network structure.
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