ArticleMolecular biology of the cell2015
Modulation of receptor dynamics by the regulator of G protein signaling Sst2.
Article in Molecular biology of the cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Design patterns of biological cells.BioEssays : news and reviews in molecular, cellular and developmental biology · 2024Review
- Orientation of Cell Polarity by Chemical Gradients.Annual review of biophysics · 2022Review
- A systems approach to investigate GPCR-mediated Ras signaling network in chemoattractant sensing.Molecular biology of the cell · 2022Article
- A predictive model of gene expression reveals the role of network motifs in the mating response of yeast.Science signaling · 2021Article
- Quantitative analysis of the yeast pheromone pathway.Yeast (Chichester, England) · 2019Article
- Tracking yeast pheromone receptor Ste2 endocytosis using fluorogen-activating protein tagging.Molecular biology of the cell · 2018Article
- Spatial and temporal signal processing and decision making by MAPK pathways.The Journal of cell biology · 2017Review
- Yeast GPCR signaling reflects the fraction of occupied receptors, not the number.Molecular systems biology · 2016Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
G protein-coupled receptor (GPCR) signaling is fundamental to physiological processes such as vision, the immune response, and wound healing. In the budding yeast Saccharomyces cerevisiae, GPCRs detect and respond to gradients of pheromone during mating. After pheromone stimulation, the GPCR Ste2 is removed from the cell membrane, and new receptors are delivered to the growing edge. The regulator of G protein signaling (RGS) protein Sst2 acts by accelerating GTP hydrolysis and facilitating pathway desensitization. Sst2 is also known to interact with the receptor Ste2. Here we show that Sst2 is required for proper receptor recovery at the growing edge of pheromone-stimulated cells. Mathematical modeling suggested pheromone-induced synthesis of Sst2 together with its interaction with the receptor function to reestablish a receptor pool at the site of polarized growth. To validate the model, we used targeted genetic perturbations to selectively disrupt key properties of Sst2 and its induction by pheromone. Together our results reveal that a regulator of G protein signaling can also regulate the G protein-coupled receptor. Whereas Sst2 negatively regulates G protein signaling, it acts in a positive manner to promote receptor retention at the growing edge.
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Registered trials
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.