<i>Arabidopsis DND2</i>, a Second Cyclic Nucleotide-Gated Ion Channel Gene for Which Mutation Causes the “<i>Defense, No Death</i>” Phenotype

Jurkowski, Grace I.; Smith, Roger K.; Yu, I-ching; Ham, Jong Hyun; Sharma, Sandeep; Klessig, Daniel F.; Fengler, Kevin; Bent, Andrew F.

doi:10.1094/mpmi.2004.17.5.511

Cited by 182 publications

(176 citation statements)

References 79 publications

Supporting

Mentioning

164

Contrasting

Unclassified

Order By: Relevance

“…Alternatively, MEKK1 kinase activity may contribute both to HR cell death and to the susceptibility-associated cell death caused by virulent P. syringae. Cell death phenotypes are separable from SA-mediated responses, for example in Arabidopsis dnd1 (cngc2) and dnd2 (hlm1/cngc4) mutants that continue to exhibit suppression of HR cell death despite removal of SAmediated responses by nahG expression or eds16 mutation (Yu et al, 1998;Jurkowski et al, 2004). Precedent for a MAP3K mediating the cell death associated with both immunity and disease susceptibility has been established (del Pozo et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

MEKK1 Is Required for flg22-Induced MPK4 Activation in Arabidopsis Plants

et al. 2006

Self Cite

View full text Add to dashboard Cite

The Arabidopsis (Arabidopsis thaliana) gene MEKK1 encodes a mitogen-activated protein kinase kinase kinase that has been implicated in the activation of the map kinases MPK3 and MPK6 in response to the flagellin elicitor peptide flg22. In this study, analysis of plants carrying T-DNA knockout alleles indicated that MEKK1 is required for flg22-induced activation of MPK4 but not MPK3 or MPK6. Experiments performed using a kinase-impaired version of MEKK1 (K361M) showed that the kinase activity of MEKK1 may not be required for flg22-induced MPK4 activation or for other macroscopic FLS2-mediated responses. MEKK1 may play a structural role in signaling, independent of its protein kinase activity. mekk1 knockout mutants display a severe dwarf phenotype, constitutive callose deposition, and constitutive expression of pathogen response genes. This dwarf phenotype was largely rescued by introduction into mekk1 knockout plants of either the MEKK1 (K361M) construct or a nahG transgene that degrades salicylic acid. When treated with pathogenic bacteria, the K361M plants were slightly more susceptible to an avirulent strain of Pseudomonas syringae and showed a delayed hypersensitive response, suggesting a role for MEKK1 kinase activity in this aspect of plant disease resistance. Our results indicate that MEKK1 acts upstream of MPK4 as a negative regulator of pathogen response pathways, a function that may not require MEKK1's full kinase activity.

show abstract

Section: Discussionmentioning

confidence: 99%

MEKK1 Is Required for flg22-Induced MPK4 Activation in Arabidopsis Plants

et al. 2006

Self Cite

View full text Add to dashboard Cite

show abstract

“…S7), suggesting that these 12 genes probably are direct targets of TPR1. Among the 12 genes identified, Defense no Death 1 (DND1) and Defense no Death 2 (DND2) are known negative regulators of plant innate immunity (22)(23)(24). ChIP followed by semiquantitative PCR also showed that TPR1 was recruited to the promoters of DND1 and DND2 (Fig.…”

Section: Tpr1 Functions As a Transcriptional Corepressor And Associatmentioning

confidence: 95%

Arabidopsis resistance protein SNC1 activates immune responses through association with a transcriptional corepressor

Zhu

Zhang

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

216

247

View full text Add to dashboard Cite

In both plants and animals, nucleotide-binding (NB) domain and leucine-rich repeat (LRR)-containing proteins (NLR) function as sensors of pathogen-derived molecules and trigger immune responses. Although NLR resistance (R) proteins were first reported as plant immune receptors more than 15 years ago, how these proteins activate downstream defense responses is still unclear. Here we report that the Toll-like/interleukin-1 receptor (TIR)-NB-LRR R protein, suppressor of npr1-1, constitutive 1 (SNC1) functions through its associated protein, Topless-related 1 (TPR1). Knocking out TPR1 and its close homologs compromises immunity mediated by SNC1 and several other TIR-NB-LRR-type R proteins, whereas overexpression of TPR1 constitutively activates SNC1-mediated immune responses. TPR1 functions as a transcriptional corepressor and associates with histone deacetylase 19 in vivo. Among the target genes of TPR1 are Defense no Death 1 (DND1) and Defense no Death 2 (DND2), two known negative regulators of immunity that are repressed during pathogen infection, suggesting that TPR1 activates R protein-mediated immune responses through repression of negative regulators.histone deacetylase 19 | plant immunity | Topless | Topless-related 1 P lant resistance (R) proteins play important roles in defense against pathogens. The majority of R proteins contain either a Toll-like/interleukin 1 receptor (TIR) or a coiled coil (CC) domain at their N terminus domain, a central nucleotide-binding (NB) domain, and C-terminal leucine-rich repeats (LRRs). Downstream components for TIR-and CC-NB-LRR R proteins appear to be different. Mutations in enhanced disease susceptibility 1 (EDS1), phytoalexin deficient 4 (PAD4), and senescence-associated gene101 (SAG101) affect the resistance specified by TIR-NB-LRR but not by CC-NB-LRR R proteins (1-3). On the other hand, mutations in non-race-specific disease resistance 1 (NDR1) compromise resistance mediated by CC-NB-LRR but not by TIR-NB-LRR R proteins (1, 4). EDS1, PAD4, and SAG101 encode three related proteins with homology to acyl hydrolases (3,5,6). How these proteins regulate R protein signaling is not clear.Increasing evidence suggests that certain R proteins accumulate in the nucleus and that the nuclear pools of these R proteins are important for the activation of defense responses (7-10). Multiple TIR-NB-LRR R proteins, including nicotiana glutinosa virus resistance protein (N) in tobacco and resistance to Pseudomonas syringae 4 (RPS4) and suppressor of npr1-1, constitutive 1 (SNC1) in Arabidopsis, have been shown to localize to the nucleus, and reduction of the nuclear R protein pool attenuates the activation of downstream defense responses (7-10). These findings are consistent with that the nucleocytoplasmic trafficking machinery is required for R protein-mediated immunity (9,11,12). However, the function of these R proteins in the nucleus and whether they participate directly or indirectly in transcriptional regulation of defense genes is unclear.Despite tremendous progress has been made ...

show abstract

“…RNA blotting and probe labeling protocols followed the procedures described by Mercier et al (2004). Primers for the PR1 probes were amplified using primers 5#-GTAGGTGCTCT-TGTTCTTCCC-3# and 5#-CACATAATTCCCACGAGGATC-3# as described by Jurkowski et al (2004).…”

Section: Lipid Peroxidationmentioning

confidence: 99%

Leaf Senescence Signaling: The Ca2+-Conducting Arabidopsis Cyclic Nucleotide Gated Channel2 Acts through Nitric Oxide to Repress Senescence Programming

Smigel

Walker

et al. 2010

Plant Physiology

View full text Add to dashboard Cite

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.

show abstract

Arabidopsis DND2, a Second Cyclic Nucleotide-Gated Ion Channel Gene for Which Mutation Causes the “Defense, No Death” Phenotype

Cited by 182 publications

References 79 publications

MEKK1 Is Required for flg22-Induced MPK4 Activation in Arabidopsis Plants

MEKK1 Is Required for flg22-Induced MPK4 Activation in Arabidopsis Plants

Arabidopsis resistance protein SNC1 activates immune responses through association with a transcriptional corepressor

Leaf Senescence Signaling: The Ca2+-Conducting Arabidopsis Cyclic Nucleotide Gated Channel2 Acts through Nitric Oxide to Repress Senescence Programming

Contact Info

Product

Resources

About