The disease-resistant Arabidopsis thaliana aberrant growth and death2 ( agd2-1 ) mutant has elevated levels of the defense signal salicylic acid (SA), altered leaf morphology, and mild dwarfism. AGD2 and its close homolog ALD1 (for AGD2-LIKE DEFENSE RESPONSE PROTEIN1 ) encode aminotransferases that act on an overlapping set of amino acids in vitro. However, kinetic parameters indicate that AGD2 and ALD1 may drive the aminotransferase reaction in opposite directions. ALD1-deficient mutants have the opposite phenotypes from agd2-1 , showing reduced SA production and increased disease susceptibility. Furthermore, ALD1 transcript levels are elevated in agd2-1 and are induced in the wild type by bacterial pathogen infection. ALD1 is responsible for some of the elevated SA content and a majority of the disease resistance and dwarfism of agd2-1 . A complete knockout of AGD2 renders embryos inviable. We suggest that AGD2 synthesizes an important amino acid–derived molecule that promotes development and suppresses defenses, whereas ALD1 generates a related amino acid–derived molecule important for activating defense signaling.
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