<p>Autophagy is a vital cellular quality control pathway that maintains cellular homoeostasis under changing environments. While the organismal phenotypes of autophagy-deficient plants under stress are well characterized, the contribution of cell-type-specific autophagy responses to whole-plant homoeostasis remains poorly understood. Here we show that root-hair-forming cells (trichoblasts) in <i>Arabidopsis thaliana</i> exhibit higher autophagic flux than adjacent non-hair cells (atrichoblasts). This differential autophagy is genetically linked to cell fate determination during early development. Mutants with disrupted trichoblast or atrichoblast identity lose the autophagy distinction between these cell types. Functional analyses reveal that elevated autophagy in trichoblasts is essential for sodium ion sequestration in vacuoles—a key mechanism for salt stress tolerance. Disrupting autophagy specifically in trichoblasts impairs sodium accumulation and reduces plant survival under salt stress. Conversely, cell-type-specific complementation restores both sodium sequestration and stress tolerance. Our findings uncover a cell-type-specific autophagy program in root hairs and demonstrate how developmental cues shape autophagy to enhance stress resilience. This work establishes a direct link between cell identity, autophagy and environmental adaptation in plants.</p>