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Multiple pathways of endocytosis have been identified in animal systems which vary in terms of the molecular constituents involved and also by the type of cargo that is internalized. Most of these studies have utilized isolated cells in culture, which undermine the possibility that endocytic mechanisms may vary across different cell types in an intact, functional tissue and, moreover, be subject to differential regulation in response to diverse physiological conditions. I have looked at different pathways of endocytosis through  different layers of the Arabidopsis root using three classes of probes: a lipophilic dye, tagged transmembrane proteins, and a lipid-anchored protein. Genetic and pharmacological perturbations of endocytic regulators indicate that at least two distinct mechanisms of endocytosis are constitutively operative: a clathrin-dependent pathway which endocytose transmembrane proteins across all cell layers; and an  epidermally restricted, sterol-dependent, clathrin-independent pathway that takes up  lipid and lipid-anchored proteins but not transmembrane proteins. NaCl stress induces a third pathway which is clathrin-independent, non-specific in its choice of cargo, and operates across all layers of the root. The Rab-GEF vps9a is an essential component of only this induced pathway. I observe the expansion of small acidic  compartments into larger vacuole-like structures in inner cell layers under saline stress. This correlates with salt-resistance, since the disruption of this expansion of vacuolar system in a vps9a mutant results in hypersensitivity to salt. Thus saline  stress reprogrammes endocytic pathways and remodels a vital compartment involved in intracellular trafficking.