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Arabidopsis hot2 encodes an endochitinase‐like protein that is essential for tolerance to heat, salt and drought stresses
Author(s) -
Kwon YeRim,
Kim SunHee,
Jung MoonSoo,
Kim MiSook,
Oh JeeEun,
Ju HyunWoo,
Kim Kangil,
Vierling Elizabeth,
Lee Hojoung,
Hong SukWhan
Publication year - 2007
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/j.1365-313x.2006.02950.x
Subject(s) - arabidopsis , mutant , overproduction , chitinase , abiotic stress , biology , microbiology and biotechnology , gene , arabidopsis thaliana , wild type , drought tolerance , biochemistry , botany
Summary 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.