Mechanical stress impairs pheromone signaling via Pkc1-mediated regulation of the MAPK scaffold Ste5.

Détails

ID Serval
serval:BIB_D75D344EEE3C
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Mechanical stress impairs pheromone signaling via Pkc1-mediated regulation of the MAPK scaffold Ste5.
Périodique
The Journal of cell biology
Auteur(s)
van Drogen F., Mishra R., Rudolf F., Walczak M.J., Lee S.S., Reiter W., Hegemann B., Pelet S., Dohnal I., Binolfi A., Yudina Z., Selenko P., Wider G., Ammerer G., Peter M.
ISSN
1540-8140 (Electronic)
ISSN-L
0021-9525
Statut éditorial
Publié
Date de publication
02/09/2019
Peer-reviewed
Oui
Volume
218
Numéro
9
Pages
3117-3133
Langue
anglais
Notes
Publication types: Journal Article
Publication Status: ppublish
Résumé
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.
Pubmed
Web of science
Open Access
Oui
Création de la notice
19/08/2019 10:33
Dernière modification de la notice
23/10/2019 5:13
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