Seminars

The eukaryotic Endoplasmic reticulum (ER)-Plasma membrane (PM) Contact Site (EPCS) are evolutionarily conserved structures involved in Ca2+ homeostasis regulation, non-vesicular lipid transport, and cell signaling. In plants, EPCS are known to regulate Ca2+-dependent responses to high salinity but the molecular mechanisms underlying their establishment and dynamics remain largely unknown. In this talk, I will discuss cytoskeleton-dependent and independent mechanisms involved in the delivery and distribution of EPCS-localized protein tethers, I will define ionic stress as a physiological trigger that induces EPCS remodeling, and I will present a model in which stress-induced phosphoinositide accumulations at the PM activate the docking of EPCS-localized tethers and the generation of expanded EPCS. These results illustrate the complex regulation of EPCS remodeling in plants, and highlight important mechanistic differences between the fast (within seconds) EPCS expansions driven by store operated Ca2+ entry widely reported in mammalian cells, and the slow EPCS expansions (within hours) driven by sustained exposure to ionic stress in plant cells.