Protein homeostasis and inter-organellar signaling under salt stress

Abstract

Abstract Salinity is a major abiotic constraint on plant growth, productivity, and global food security. It disrupts cellular protein homeostasis (proteostasis) at every step, from synthesis to degradation. Plant survival under salt stress therefore depends on the coordinated regulation of protein synthesis, folding, post-translational modification, trafficking, quality control, and turnover. The individual contributions of the nucleus, ribosomes, endoplasmic reticulum (ER), and Golgi apparatus to salinity responses are increasingly well described, but how these compartments communicate remains far less understood. This review synthesizes current evidence on this inter-organellar signaling network, addressing four questions: how salinity-induced osmotic, ionic, and oxidative stress reprograms nuclear transcription and chromatin state; how ribosomes sustain selective translation of protective proteins while clearing stalled or damaged translational products; how the ER expands its folding capacity through the unfolded protein response and removes terminally misfolded proteins by ER-associated degradation; and how the Golgi sustains glycosylation, sorting, and secretion of the transporters needed for ion and osmotic homeostasis. Beyond these organelle-level responses, the review discusses two signaling layers that couple them into a single circuit: post-translational modifications (phosphorylation, ubiquitination, SUMOylation, and redox- and nitrosative/persulfidation-based marks) and phytohormone/gasotransmitter signals, including abscisic acid, nitric oxide, hydrogen sulfide, carbon monoxide, and melatonin. By framing proteostasis as an emergent property of nucleus-ribosome-ER-Golgi coordination rather than of any single compartment, this review identifies specific inter-organellar signaling nodes as candidate targets for breeding or engineering salinity-resilient crops.