ArticleThe Journal of cell biology2019
Mechanical stress impairs pheromone signaling via Pkc1-mediated regulation of the MAPK scaffold Ste5.
Article in The Journal of cell biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 22 citations in OpenAlex.
- 3D confinement physically regulates cell cycle progression in budding yeast.Nature communications · 2026Article
- Regulation of the Cell Wall Integrity pathway at the contact site between mating partners in yeast.The Journal of cell biology · 2026Article
- Phosphoregulation of the novel hemi-arrestin MAPK scaffold Sms1 prevents untimely mating.Nature communications · 2026Article
- Normal stress on surface of mesenchymal stem cells boosts extracellular vesicle secretion and regenerative bioactivity.Journal of nanobiotechnology · 2025Article
- Combinatorial phosphorylation modulates the structure and function of the G protein γ subunit in yeast.Science signaling · 2021Article
- Crosstalk and spatiotemporal regulation between stress-induced MAP kinase pathways and pheromone signaling in budding yeast.Cell cycle (Georgetown, Tex.) · 2020Review
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Authors and funding
15 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cells continuously adapt cellular processes by integrating external and internal signals. In yeast, multiple stress signals regulate pheromone signaling to prevent mating under unfavorable conditions. However, the underlying crosstalk mechanisms remain poorly understood. Here, we show that mechanical stress activates Pkc1, which prevents lysis of pheromone-treated cells by inhibiting polarized growth. In vitro Pkc1 phosphorylates conserved residues within the RING-H2 domains of the scaffold proteins Far1 and Ste5, which are also phosphorylated in vivo. Interestingly, Pkc1 triggers dispersal of Ste5 from mating projections upon mechanically induced stress and during cell-cell fusion, leading to inhibition of the MAPK Fus3. Indeed, RING phosphorylation interferes with Ste5 membrane association by preventing binding to the receptor-linked Gβγ protein. Cells expressing nonphosphorylatable Ste5 undergo increased lysis upon mechanical stress and exhibit defects in cell-cell fusion during mating, which is exacerbated by simultaneous expression of nonphosphorylatable Far1. These results uncover a mechanical stress-triggered crosstalk mechanism modulating pheromone signaling, polarized growth, and cell-cell fusion during mating.
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