Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Arabidopsis thaliana SSI2 gene encodes a plastid-localized stearoyl-ACP desaturase. The recessive ssi2 mutant allele confers constitutive accumulation of the pathogenesis-related-1 (PR-1) gene transcript and salicylic acid (SA), and enhanced resistance to bacterial and oomycete pathogens. In addition, the ssi2 mutant is a dwarf and spontaneously develops lesions containing dead cells. Here, we show that the ssi2 mutant also confers enhanced resistance to Cucumber mosaic virus (CMV). Compared with the wild-type plant, viral multiplication and systemic spread were diminished in the ssi2 mutant plant. However, unlike the ssi2-conferred resistance to bacterial and oomycete pathogens, the ssi2-conferred enhanced resistance to CMV was retained in the SA-deficient ssi2 nahG plant. In addition, SA application was not effective in limiting CMV multiplication and systemic spread in the CMV-susceptible wild-type plant. The acd1, acd2, and cpr5 mutants which, like the ssi2 mutant, accumulate elevated SA levels, constitutively express the PR-1 gene, spontaneously develop lesions containing dead cells, and are dwarfs, are, however, fully susceptible to CMV. Our results suggest that dwarfing, cell death, and constitutive activation of SA signaling are not important for the ssi2-conferred enhanced resistance to CMV. However, the sfd1 and sfd4 mutations, which affect lipid metabolism, suppress the ssi2-conferred enhanced resistance to CMV, thus implicating a lipid or lipids in the ssi2-conferred resistance to CMV. Interestingly, the ssi2-conferred resistance to CMV was compromised in the ssi2 eds5 plant, suggesting the involvement of an SA-independent, EDS5-dependent mechanism in the ssi2-conferred resistance to CMV.
Mol Plant Microbe Interact 2004 Jun
PMID:Enhanced resistance to Cucumber mosaic virus in the Arabidopsis thaliana ssi2 mutant is mediated via an SA-independent mechanism. 1519 45

Loss of a stearoyl-ACP desaturase activity in the Arabidopsis thaliana ssi2 mutant confers susceptibility to the necrotroph, Botrytis cinerea. In contrast, the ssi2 mutant exhibits enhanced resistance to Pseudomonas syringae, Peronospora parasitica, and Cucumber mosaic virus. The altered basal resistance to these pathogens in the ssi2 mutant plant is accompanied by the constitutive accumulation of elevated salicylic acid (SA) level and expression of the pathogenesis-related 1 (PR1) gene, the inability of jasmonic acid (JA) to activate expression of the defensin gene, PDF1.2, and the spontaneous death of cells. Here, we show that presence of the eds5 and pad4 mutant alleles compromises the ssi2-conferred resistance to Pseudomonas syringae pv. maculicola. In contrast, resistance to B. cinerea was restored in the ssi2 eds5 and ssi2 pad4 double-mutant plants. However, resistance to B. cinerea was not accompanied by the restoration of JA responsiveness in the ssi2 eds5 and ssi2 pad4 plants. The ssi2 eds5 and ssi2 pad4 plants retain the ssi2-conferred spontaneous cell death phenotype, suggesting that cell death is not a major factor that predisposes the ssi2 mutant to infection by B. cinerea. Furthermore, the high SA content of the ssi2 pad4 plant, combined with our previous observation that the SA-deficient ssi2 nahG plant succumbs to infection by B. cinerea, suggests that elevated SA level does not have a causal role in the ssi2-conferred susceptibility to B. cinerea. Our results suggest that interaction between an SSI2-dependent factor or factors and an EDS5- and PAD4-dependent mechanism or mechanisms modulates defense to B. cinerea.
Mol Plant Microbe Interact 2005 Apr
PMID:Arabidopsis ssi2-conferred susceptibility to Botrytis cinerea is dependent on EDS5 and PAD4. 1582 88

The lesion-mimic Arabidopsis mutant, syp121 syp122, constitutively expresses the salicylic acid (SA) signaling pathway and has low penetration resistance to powdery mildew fungi. Genetic analyses of the lesion-mimic phenotype have expanded our understanding of programmed cell death (PCD) in plants. Inactivation of SA signaling genes in syp121 syp122 only partially rescues the lesion-mimic phenotype, indicating that additional defenses contribute to the PCD. Whole genome transcriptome analysis confirmed that SA-induced transcripts, as well as numerous other known pathogen-response transcripts, are up-regulated after inactivation of the syntaxin genes. A suppressor mutant analysis of syp121 syp122 revealed that FMO1, ALD1, and PAD4 are important for lesion development. Mutant alleles of EDS1, NDR1, RAR1, and SGT1b also partially rescued the lesion-mimic phenotype, suggesting that mutating syntaxin genes stimulates TIR-NB-LRR and CC-NB-LRR-type resistances. The syntaxin double knockout potentiated a powdery mildew-induced HR-like response. This required functional PAD4 but not functional SA signaling. However, SA signaling potentiated the PAD4-dependent HR-like response. Analyses of quadruple mutants suggest that EDS5 and SID2 confer separate SA-independent signaling functions, and that FMO1 and ALD1 mediate SA-independent signals that are NPR1-dependent. These studies highlight the contribution of multiple pathways to defense and point to the complexity of their interactions.
Mol Plant 2008 May
PMID:A lesion-mimic syntaxin double mutant in Arabidopsis reveals novel complexity of pathogen defense signaling. 1982 57

The ascorbic acid (AA)-deficient Arabidopsis thaliana vtc1-1 mutant exhibits increased resistance to the virulent bacterial pathogen Pseudomonas syringae. This response correlates with heightened levels of salicylic acid (SA), which induces antimicrobial pathogenesis-related (PR) proteins. To determine if SA-mediated, enhanced disease resistance is a general phenomenon of AA deficiency, to elucidate the signal that stimulates SA synthesis, and to identify the biosynthetic pathway through which SA accumulates, we studied the four AA-deficient vtc1-1, vtc2-1, vtc3-1, and vtc4-1 mutants. We also studied double mutants defective in the AA-biosynthetic gene VTC1 and the SA signaling pathway genes PAD4, EDS5, and NPR1, respectively. All vtc mutants were more resistant to P. syringae than the wild type. With the exception of vtc4-1, this correlated with constitutively upregulated H(2)O(2), SA, and messenger RNA levels of PR genes. Double mutants exhibited decreased SA levels and enhanced susceptibility to P. syringae compared with the wild type, suggesting that vtc1-1 requires functional PAD4, EDS5, and NPR1 for SA biosynthesis and pathogen resistance. We suggest that AA deficiency causes constitutive priming through a buildup of H(2)O(2) that stimulates SA accumulation, conferring enhanced disease resistance in vtc1-1, vtc2-1, and vtc3-1, whereas vtc4-1 might be sensitized to H(2)O(2) and SA production after infection.
Mol Plant Microbe Interact 2010 Mar
PMID:Ascorbic acid deficiency in arabidopsis induces constitutive priming that is dependent on hydrogen peroxide, salicylic acid, and the NPR1 gene. 2012 55