Disease relevance of Camalexin

• The Arabidopsis PAD4 gene was previously shown to be required for synthesis of camalexin in response to infection by the virulent bacterial pathogen Pseudomonas syringae pv maculicola ES4326 but not in response to challenge by the non-host fungal pathogen Cochliobolus carbonum [1].
• Production of disease symptoms is not sufficient for the response because systemic infection with cauliflower mosaic virus or cucumber mosaic virus did not induce the tryptophan pathway enzymes or camalexin accumulation [2].
• Both PAD4 and NahG acted epistatically to SID regarding the Pst-dependent production of ET that was found to be necessary for the accumulation of camalexin [3].
• Assays of membrane integrity revealed that, like other phytoalexins, camalexin disrupts bacterial membranes, suggesting that camalexin toxicity is a consequence of membrane disruption [4].
• The virulent Arabidopsis thaliana pathogen Pseudomonas syringae pv. maculicola strain ES4326 (Psm ES4326) and other gram-negative bacteria are sensitive to camalexin (3-thiazol-2'-yl-indole), the Arabidopsis phytoalexin [4].

High impact information on Camalexin

• Arabidopsis PAD3, a gene required for camalexin biosynthesis, encodes a putative cytochrome P450 monooxygenase [5].
• Salicylic acid induction-deficient mutants of Arabidopsis express PR-2 and PR-5 and accumulate high levels of camalexin after pathogen inoculation [6].
• The expression of PAD3 is tightly correlated with camalexin synthesis and is regulated by PAD4 and PAD1 [5].
• In this study, we show that pad4 mutants exhibit defects in defense responses, including camalexin synthesis and pathogenesis-related PR-1 gene expression, when infected by P. s. maculicola ES4 326 [1].
• Moreover, treatment of pad4 plants with SA partially reversed the camalexin deficiency and PR-1 gene expression phenotypes of P. s. maculicola ES4 326-infected pad4 plants [1].

Biological context of Camalexin

• It was previously shown that camalexin accumulation is caused by infection with plant pathogens, by abiotic elicitors, and in spontaneous lesions in the accelerated cell death mutant acd2 [2].
• NahG was shown to act epistatically to the sid mutant phenotype regarding accumulation of camalexin after inoculation with Pst in eds5NahG and sid2NahG plants [3].
• Surprisingly, in both pathosystems, the disease susceptibility of pad2-1 was not caused by the camalexin deficiency, suggesting additional roles of PAD2 in disease resistance [7].
• Botrytis cinerea isolates showed differing sensitivity to purified camalexin, and camalexin-sensitive isolates produced larger lesions on camalexin-deficient Arabidopsis genotypes than on the wild type [8].
• Camalexin accumulation in ups1 is greatly reduced after infection with these two pathogens, as well as after amino acid starvation or oxidative stress [9].

Anatomical context of Camalexin

• We also demonstrate that a variety of resistance-associated phenomena, including the TCV-induced accumulation of salicylic acid, camalexin and autofluorescent cell-wall material, correlate with the HR, suggesting the possibility that HRT is required for their activation [10].
• CYP71B15 catalyses the final step in camalexin biosynthesis, as recombinant CYP71B15 and microsomes from Arabidopsis leaves expressing functional PAD3 converted dihydrocamalexic acid into camalexin [11].

Associations of Camalexin with other chemical compounds

• Furthermore, production of camalexin in the sur1 mutant devoid of glucosinolates excludes the possibility that camalexin is derived from indole glucosinolates [12].
• Origin of the thiazole ring of camalexin, a phytoalexin from Arabidopsis thaliana [13].
• Cys labeled either with deuterium (D3-Cys[2,3,3]) or 13C and 15N ([U-13C,15N]Cys) was also fed to inoculated leaves of Arabidopsis; camalexin was analyzed by mass spectroscopic analysis [13].
• Resistance is compromised by pad3 or coi1 mutations, suggesting that it requires the Arabidopsis phytoalexin camalexin and jasmonic acid (JA)-dependent signaling, respectively [14].
• Metabolic changes during NOD-induced senescence comprehended increases in salicylic acid (SA) levels, accumulation of the phytoalexin camalexin and elevation of leaf gamma-tocopherol contents, all of which occurred during natural senescence in Arabidopsis leaves as well [15].

Gene context of Camalexin

• The Arabidopsis PAD4 gene previously was found to be required for expression of multiple defense responses including camalexin synthesis and PR-1 gene expression in response to infection by the bacterial pathogen Pseudomonas syringae pv. maculicola [16].
• These results demonstrate that only CYP79B2 and CYP79B3 contribute significantly to the IAOx pool from which camalexin and indole glucosinolates are synthesized [12].
• We are working to determine the role of the Arabidopsis phytoalexin, camalexin, in protecting the plant from pathogen attack by isolating phytoalexin-deficient (pad) mutants in the accession Columbia (Col-0) and examining their response to pathogens [17].
• Moreover, the expression of BABA-induced resistance was not associated with enhanced accumulation of camalexin or enhanced transcription of the JA-inducible PDF1.2 gene [18].
• The biosynthesis of camalexin, the main phytoalexin of the model plant Arabidopsis thaliana, involves at least two CYP (cytochrome P450) steps [11].
• Together, these results lead to the conclusion that CYP71A13 catalyzes the conversion of IAOx to IAN in camalexin synthesis and provide further support for the role of camalexin in resistance to A. brassicicola [19].

Analytical, diagnostic and therapeutic context of Camalexin

• TLC plate bioassays suggested that A. brassicicola was relatively insensitive to camalexin, thus casting some doubt on the importance of this compound in defense [20].

References