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

Abstract

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.

The Ankyrin-Repeat Transmembrane Protein BDA1 Functions Downstream of the Receptor-Like Protein SNC2 to Regulate Plant Immunity

“…bda1-17D has very similar mutant phenotypes to acd6-1, which also exhibits spontaneous cell death, expresses high levels of PR-1, and displays enhanced pathogen resistance (Rate et al, 1999). Interestingly, the gain-of-function mutation in acd6-1 also occurs in one of the transmembrane domains (Lu et al, 2003).…”

HLM1, an Essential Signaling Component in the Hypersensitive Response, Is a Member of the Cyclic Nucleotide–Gated Channel Ion Channel Family[W]

“…These mutants provide the opportunity to dissect the defense signaling pathways and the communication between multiple pathways that might not be available by studying the responses of wild-type plants to pathogens. Thus, among the different lesion-mimic mutants identified to date, some of them present a normal HR (all of the lsd mutants except lsd1, acd5, cpr22, and dll1) (Dietrich et al, 1994;Greenberg et al, 2000;Yoshioka et al, 2001;Pilloff et al, 2002), one of them exhibits an accelerated HR (cpn1) (Jambunathan et al, 2001), some of them show runaway cell death (lsd1 and acd2) (Dietrich et al, 1994;Greenberg et al, 1994), and some others show a suppressed HR phenotype (dnd1, acd6, agd2, and hrl1) (Yu et al, 1998;Rate et al, 1999;Rate and Greenberg, 2001;Devadas and Raina, 2002). Among these mutants, lesion formation can be either nahG and/or NPR dependent or nahG and/or NPR independent (lsd2, lsd4, cpr5, and ssi2) (Bowling et al, 1997;Hunt et al, 1997;Shah et al, 2001).…”

“…Mutants that show a similar phenotype (spontaneous lesions and HR suppression) have been isolated (Yu et al, 1998;Rate et al, 1999;Rate and Greenberg, 2001), including the dnd mutants. One of their corresponding genes, DND1, has been cloned and encodes a CNGC, CNGC2.…”

Expansive Phenotypic Landscape of Botrytis cinerea Shows Differential Contribution of Genetic Diversity and Plasticity

“…Leaves were infected as described above and were stained as previously described (Rate et al 1999;van Wees 2008). Isolate-specific differences were observed in the relative hyphal density, DVB, and the tendency to develop exploratory hyphae and to leaf vasculature.…”