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In plants, salicylic acid (SA) plays important roles in regulating immunity and programed cell death. Early studies revealed that increased SA accumulation is associated with the onset of hypersensitive reaction during resistance gene-mediated defense responses. SA was also found to accumulate to high levels in lesion-mimic mutants and in some cases the accumulation of SA is required for the spontaneous cell death phenotype. Meanwhile, high levels of SA have been shown to negatively regulate plant cell death during effector-triggered immunity, suggesting that SA has dual functions in cell death control. The molecular mechanisms of how SA regulates cell death in plants are discussed.

Membrane contact sites between the cortical endoplasmic reticulum (ER) and the plasma membrane (PM) provide a direct conduit for small molecule transfer and signaling between the two largest membranes of the cell. Contact is established through ER integral membrane proteins that physically tether the two membranes together, though the general mechanism is remarkably non-specific given the diversity of different tethering proteins. Primary tethers including VAMP-associated proteins (VAPs), Anoctamin/TMEM16/Ist2p homologs, and extended synaptotagmins (E-Syts), are largely conserved in most eukaryotes and are both necessary and sufficient for establishing ER-PM association. In addition, other species-specific ER-PM tether proteins impart unique functional attributes to both membranes at the cell cortex. This review distils recent functional and structural findings about conserved and speciesspecific tethers that form ER-PM contact sites, with an emphasis on their roles in the coordinate regulation of lipid metabolism, cellular structure, and responses to membrane stress.

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