The Arabidopsis gain‐of‐function mutant dll1 spontaneously develops lesions mimicking cell death associated with disease

Abstract

SummaryWe describe the characterization of a novel gain-of-function Arabidopsis mutant, dll1 (disease-like lesions1), which spontaneously develops lesions mimicking bacterial speck disease and constitutively expresses biochemical and molecular markers associated with pathogen infection. Despite the constitutive expression of defense-related responses, dll1 is unable to suppress the growth of virulent pathogens. However, dll1 elicits normal hypersensitive response in response to avirulent pathogens, thus indicating that dll1 is not defective in the induction of normal resistance responses. The lesion + leaves of dll1 support the growth of hrcC mutant of Pseudomonas syringae, which is defective in the transfer of virulence factors into the plant cells, and therefore non-pathogenic to wild-type Col-0 plants. This suggests that dll1 intrinsically expresses many of the cellular processes that are required for pathogen growth during disease. Epistasis analyses reveal that salicylic acid and NPR1 are required for lesion formation, while ethylene modulates lesion development in dll1, suggesting that signi®cant overlap exist between the signalling pathways leading to resistance-and disease-associated cell death. Our results suggest that host cell death during compatible interactions, at least in part, is genetically controlled by the plant and DLL1 may positively regulate this process.

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).…”

VASCULAR ASSOCIATED DEATH1, a Novel GRAM Domain–Containing Protein, Is a Regulator of Cell Death and Defense Responses in Vascular Tissues

“…We identified a novel lesion mimic mutant, vad1, which exhibits propagative HR-like lesions along the vascular system. To our knowledge, only five other propagation mutants have been isolated to date, and among them two exhibit disease-like (not HR-like) lesions (Brodersen et al, 2002;Pilloff et al, 2002); therefore, vad1 may be a new function involved in cell death control. The observations that (1) the mutant constitutively expresses defense genes, accumulates elevated levels of SA, and exhibits enhanced resistance to P. syringae and (2) that its phenotypes are dependent on SA accumulation, and partially or completely on the resistance components EDS1 and NDR1, are in favor of its involvement in cell death/defense pathways.…”

“…To date, among the 37 lesion mimic mutants that have been identified, only five mutants show propagative lesions: the acd (for accelerated cell death) mutants acd1 and acd2 (Greenberg and Ausubel, 1993;Greenberg et al, 1994) and the lsd1 mutant (Dietrich et al, 1994), showing necrotic, HR-like lesions, and the disease like lesion1 (dll1) and acd11 mutants, exhibiting chlorotic, disease-like lesions (Brodersen et al, 2002;Pilloff et al, 2002). These mutants, unable to control the rate and extent of the lesions, are thought to be affected in genes controlling the suppression/limitation of PCD, whereas the other lesion mimic mutants, the so-called initiation mutants, would be altered in the initiation of the process (Walbot et al, 1983).…”

Cytokinin Response Factor 2 positively regulates salicylic acid-mediated plant immunity in <i>Arabidopsis thaliana</i>

“…The expression of the bacterial NahG transgene, which encodes salicylate hydroxylase and inhibits salicylic acid accumulation, suppresses spontaneous lesion formation and autoimmune response in some lesion-mimic mutants (Brodersen et al 2005;Pilloff et al 2002). Thus, the NahG gene driven by the CaMV 35S promoter was introduced into AtCRF2-OX plants.…”