The Gain-of-Function Arabidopsis acd6 Mutant Reveals Novel Regulation and Function of the Salicylic Acid Signaling Pathway in Controlling Cell Death, Defenses, and Cell Growth

We isolated a dominant gain-of-function Arabidopsis mutant, accelerated cell death 6 ( acd6 ), with elevated defenses, patches of dead and enlarged cells, reduced stature, and increased resistance to Pseudomonas syringae . The acd6 -conferred phenotypes are suppressed by removing a key signaling molecule, salicylic acid (SA), by using the nahG transgene, which encodes SA hydroxylase. This suppression includes phenotypes that are not induced by application of SA to wild-type plants, indicating that SA acts with a second signal to cause many acd6 -conferred phenotypes. acd6–nahG plants show hyperactivation of all acd6 -conferred phenotypes after treatment with a synthetic inducer of the SA pathway, benzo(1,2,3)thiadiazole-7-carbothioic acid (BTH), suggesting that SA acts with and also modulates the levels and/or activity of the second defense signal. acd6 acts partially through a NONEXPRESSOR OF PR 1 ( NPR1 ) gene–independent pathway that activates defenses and confers resistance to P. syringae . Surprisingly, BTH-treated acd6–nahG plants develop many tumor-like abnormal growths, indicating a possible role for SA in modulating cell growth.