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Shared and redundant proteins coordinate signal cross-talk between MAPK pathways in yeast

ABSTRACT: Shared and redundant proteins coordinate signal cross-talk between MAPK pathways in yeast

PROVIDER: PRJNA1128162 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29554516_1.fastq.gz	Fastqsanger.gz
	SRR29554516_2.fastq.gz	Fastqsanger.gz
	SRR29554517_1.fastq.gz	Fastqsanger.gz
	SRR29554517_2.fastq.gz	Fastqsanger.gz
	SRR29554518_1.fastq.gz	Fastqsanger.gz

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Shared and redundant proteins coordinate signal cross-talk between MAPK pathways in yeast

Project description:All cells must detect, interpret and adapt to multiple and concurrent stimuli. While signaling pathways are highly specialized, different pathways often share components or have components with overlapping functions. In the yeast Saccharomyces cerevisiae, the high osmolarity glycerol (HOG) pathway has two seemingly redundant branches, mediated by Sln1 and Sho1. Both branches are activated by osmotic pressure, leading to phosphorylation of the MAPKs Hog1 and Kss1. The mating pathway is activated by pheromone, leading to phosphorylation of the MAPKs Fus3 and Kss1. Given that Kss1 is shared by the two pathways, we investigated its role in signal coordination. We activated both pathways with a combination of salt and pheromone, in cells lacking the shared MAPK and in cells lacking either of the redundant branches of the HOG pathway. By systematically evaluating MAPK activation, translocation, and transcription programs, we determined that Sho1 mediates cross talk between the HOG and mating pathways and does so through Kss1. Further, we show that Kss1 initiates a transcriptional program that is distinct from that induced by Hog1 and Fus3. Our findings reveal how redundant and shared components coordinate concurrent signals and thereby adapt to sudden environmental changes.

2024-06-29 | GSE270781 | GEO

Shared and redundant proteins coordinate signal cross-talk between MAPK pathways in yeast.

Project description:All cells must detect, interpret, and adapt to multiple and concurrent stimuli. While signaling pathways are highly specialized, different pathways often share components or have components with overlapping functions. In the yeast Saccharomyces cerevisiae, the high osmolarity glycerol (HOG) pathway has two seemingly redundant branches, mediated by Sln1 and Sho1. Both branches are activated by osmotic pressure, leading to phosphorylation of the MAPKs Hog1 and Kss1. The mating pathway is activated by pheromone, leading to phosphorylation of the MAPKs Fus3 and Kss1. Given that Kss1 is shared by the two pathways, we investigated its role in signal coordination. We activated both pathways with a combination of salt and pheromone, in cells lacking the shared MAPK and in cells lacking either of the redundant branches of the HOG pathway. By systematically evaluating MAPK activation, translocation, and transcription programs, we determined that Sho1 mediates cross talk between the HOG and mating pathways and does so through Kss1. Further, we show that Kss1 initiates a transcriptional program that is distinct from that induced by Hog1 and Fus3. Our findings reveal how redundant and shared components coordinate concurrent signals and thereby adapt to sudden environmental changes.

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Project description:Extracellular signal regulated kinases, ERK1 and ERK2 are often considered as redundant due to their high homology, large number of overlapping substrates, and ability to substitute for each other in genetically engineered mouse models. We have investigated the individual contribution of ERK1 and ERK2 to the survival of human melanoma cell lines driven by oncogenic BRAF. ERK2, but not ERK1 activity, was crucial to drive survival and maintain transcriptional output of the MAPK pathway. Furthermore, we found that ERK2 DEF-domain interactions were crucial for transcriptional regulation and survival in some cells, but not in others, whereas ERK2-substrate interactions at the D-docking motif were largely dispensable. We used microarrays to examine the global impact of gene expression by imhibiting different nodes of MAPK pathway.

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