Abstract:SummarySalicylic acid (SA)-dependent signaling controls activation of a set of plant defense mechanisms that are important for resistance to a variety of microbial pathogens. Many Arabidopsis mutants that display altered SA-dependent signaling have been isolated. We used double mutant analysis to determine the relative positions of the pad4, cpr1, cpr5, cpr6, dnd1 and dnd2 mutations in the signal transduction network leading to SA-dependent activation of defense gene expression and disease resistance. The pad4… Show more
“…Previous studies have reported that spontaneous necrotic lesions can appear in dnd1 leaves (Clough et al, 2000;Jirage et al, 2001). Here, our observation further expands our understanding of the dnd1 mutant phenotype.…”
Section: Resultssupporting
confidence: 82%
“…In addition to involvement in pathogenmediated Ca 2+ signaling, CNGC2 has been suggested to participate in the process of leaf development/ senescence (Kö hler et al, 2001). dnd1 mutant plants have high levels of SA and expression of PR1 (Yu et al, 1998), and spontaneous necrotic lesions appear conditionally in dnd1 leaves (Clough et al, 2000;Jirage et al, 2001). Endogenous H 2 O 2 levels in dnd1 mutants are increased from wild-type levels (Mateo et al, 2006).…”
Ca 2+ and nitric oxide (NO) are essential components involved in plant senescence signaling cascades. In other signaling pathways, NO generation can be dependent on cytosolic Ca 2+ . The Arabidopsis (Arabidopsis thaliana) mutant dnd1 lacks a plasma membrane-localized cation channel (CNGC2). We recently demonstrated that this channel affects plant response to pathogens through a signaling cascade involving Ca 2+ modulation of NO generation; the pathogen response phenotype of dnd1 can be complemented by application of a NO donor. At present, the interrelationship between Ca 2+ and NO generation in plant cells during leaf senescence remains unclear. Here, we use dnd1 plants to present genetic evidence consistent with the hypothesis that Ca 2+ uptake and NO production play pivotal roles in plant leaf senescence. Leaf Ca 2+ accumulation is reduced in dnd1 leaves compared to the wild type. Early senescence-associated phenotypes (such as loss of chlorophyll, expression level of senescence-associated genes, H 2 O 2 generation, lipid peroxidation, tissue necrosis, and increased salicylic acid levels) were more prominent in dnd1 leaves compared to the wild type. Application of a Ca 2+ channel blocker hastened senescence of detached wild-type leaves maintained in the dark, increasing the rate of chlorophyll loss, expression of a senescence-associated gene, and lipid peroxidation. Pharmacological manipulation of Ca 2+ signaling provides evidence consistent with genetic studies of the relationship between Ca 2+ signaling and senescence with the dnd1 mutant. Basal levels of NO in dnd1 leaf tissue were lower than that in leaves of wild-type plants. Application of a NO donor effectively rescues many dnd1 senescence-related phenotypes. Our work demonstrates that the CNGC2 channel is involved in Ca 2+ uptake during plant development beyond its role in pathogen defense response signaling. Work presented here suggests that this function of CNGC2 may impact downstream basal NO production in addition to its role (also linked to NO signaling) in pathogen defense responses and that this NO generation acts as a negative regulator during plant leaf senescence signaling.
“…Previous studies have reported that spontaneous necrotic lesions can appear in dnd1 leaves (Clough et al, 2000;Jirage et al, 2001). Here, our observation further expands our understanding of the dnd1 mutant phenotype.…”
Section: Resultssupporting
confidence: 82%
“…In addition to involvement in pathogenmediated Ca 2+ signaling, CNGC2 has been suggested to participate in the process of leaf development/ senescence (Kö hler et al, 2001). dnd1 mutant plants have high levels of SA and expression of PR1 (Yu et al, 1998), and spontaneous necrotic lesions appear conditionally in dnd1 leaves (Clough et al, 2000;Jirage et al, 2001). Endogenous H 2 O 2 levels in dnd1 mutants are increased from wild-type levels (Mateo et al, 2006).…”
Ca 2+ and nitric oxide (NO) are essential components involved in plant senescence signaling cascades. In other signaling pathways, NO generation can be dependent on cytosolic Ca 2+ . The Arabidopsis (Arabidopsis thaliana) mutant dnd1 lacks a plasma membrane-localized cation channel (CNGC2). We recently demonstrated that this channel affects plant response to pathogens through a signaling cascade involving Ca 2+ modulation of NO generation; the pathogen response phenotype of dnd1 can be complemented by application of a NO donor. At present, the interrelationship between Ca 2+ and NO generation in plant cells during leaf senescence remains unclear. Here, we use dnd1 plants to present genetic evidence consistent with the hypothesis that Ca 2+ uptake and NO production play pivotal roles in plant leaf senescence. Leaf Ca 2+ accumulation is reduced in dnd1 leaves compared to the wild type. Early senescence-associated phenotypes (such as loss of chlorophyll, expression level of senescence-associated genes, H 2 O 2 generation, lipid peroxidation, tissue necrosis, and increased salicylic acid levels) were more prominent in dnd1 leaves compared to the wild type. Application of a Ca 2+ channel blocker hastened senescence of detached wild-type leaves maintained in the dark, increasing the rate of chlorophyll loss, expression of a senescence-associated gene, and lipid peroxidation. Pharmacological manipulation of Ca 2+ signaling provides evidence consistent with genetic studies of the relationship between Ca 2+ signaling and senescence with the dnd1 mutant. Basal levels of NO in dnd1 leaf tissue were lower than that in leaves of wild-type plants. Application of a NO donor effectively rescues many dnd1 senescence-related phenotypes. Our work demonstrates that the CNGC2 channel is involved in Ca 2+ uptake during plant development beyond its role in pathogen defense response signaling. Work presented here suggests that this function of CNGC2 may impact downstream basal NO production in addition to its role (also linked to NO signaling) in pathogen defense responses and that this NO generation acts as a negative regulator during plant leaf senescence signaling.
“…Signi®cantly, pad4 suppressed cpr1-and cpr6-induced resistance to P.s. maculicola ES4326 and P. parasitica Noco2, and SAdependent PR gene expression (Jirage et al, 2001). Also, pad4 partially suppressed cpr5-induced pathogen resistance, but had no signi®cant effect on SA accumulation or PR gene induction.…”
Section: Salicylic Acid Signaling Antagonizes Pdf12 Expression In Cpr6mentioning
confidence: 94%
“…In contrast, eds1 only partially suppresses resistance in cpr5, leading us to conclude that cpr5 expresses both EDS1-dependent and EDS1-independent components of plant resistance. Jirage et al (2001) show in an accompanying paper that the cpr1-, cpr5-and cpr6-conditioned phenotypes have similar requirements for the SA regulatory gene PAD4 as for EDS1. We conclude that EDS1 and PAD4 have similar positions in the cpr-induced signaling cascades.…”
Section: Introductionmentioning
confidence: 92%
“…In a parallel study, Jirage et al (2001) performed genetic epistasis analysis between the SA regulatory mutant pad4 and cpr1, cpr5 and cpr6. PAD4 was found to be required for the same cpr-induced resistance phenotypes as eds1, suggesting that EDS1 and PAD4 function at a similar position in the cpr-driven signaling network.…”
Section: Salicylic Acid Signaling Antagonizes Pdf12 Expression In Cpr6mentioning
SummaryThe systemic acquired resistance (SAR) response in Arabidopsis is characterized by the accumulation of salicylic acid (SA), expression of the pathogenesis-related (PR) genes, and enhanced resistance to virulent bacterial and oomycete pathogens. The cpr (constitutive expressor of PR genes) mutants express all three SAR phenotypes. In addition, cpr5 and cpr6 induce expression of PDF1.2, a defenserelated gene associated with activation of the jasmonate/ethylene-mediated resistance pathways. cpr5 also forms spontaneous lesions. In contrast, the eds1 (enhanced disease susceptibility) mutation abolishes race-speci®c resistance conferred by a major subclass of resistance (R) gene products in response to avirulent pathogens. eds1 plants also exhibit increased susceptibility to virulent pathogens. Epistasis experiments were designed to explore the relationship between the cpr-and EDS1-mediated resistance pathways. We found that a null eds1 mutation suppresses the disease resistance phenotypes of both cpr1 and cpr6. In contrast, eds1 only partially suppresses resistance in cpr5, leading us to conclude that cpr5 expresses both EDS1-dependent and EDS1-independent components of plant disease resistance. Although eds1 does not prevent lesion formation on cpr5 leaves, it alters their appearance and reduces their spread. This phenotypic difference is associated with increased pathogen colonization of cpr5 eds1 plants compared to cpr5. The data allow us to place EDS1 as a necessary downstream component of cpr1-and cpr6-mediated responses, but suggest a more complex relationship between EDS1 and cpr5 in plant defense.
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