The Arabidopsis hot2 mutant was originally identified based on its lack of thermotolerance, but pleiotropic abnormal phenotypes are also exhibited under normal conditions, including semi-dwarfism, ethylene overproduction and aberrant cell shape with incomplete cell walls. Here we present additional characterization of the hot2 mutant, and the map-based cloning of HOT2. Mutants of hot2 had an aberrant tolerance to salt and drought stresses, and accumulated high levels of Na(+) in cells under either normal or NaCl stress conditions. Expression of the stress-inducible COR15A and KIN1 gene in hot2 mutants in response to increased NaCl concentrations was normal. HOT2 encoded a chitinase-like protein (AtCTL1) that has not previously been shown to be involved in tolerance to salt stress. Ten-day-old seedlings of wild-type plants exhibited constitutive expression of the AtCTL1 transcript, the level of which was unaffected by treatment with NaCl, mannitol or mild heat. These observations provide genetic evidence that a chitinase-like protein prevents the overaccumulation of Na(+) ions, thereby contributing to the salt tolerance in Arabidopsis. A possible role for this chitinase-like protein in Arabidopsis tolerance to abiotic stress is discussed.