Deficiency in phytoalexin production causes enhanced susceptibility of Arabidopsis thaliana to the fungus Alternaria brassicicola

Citation
Bphj. Thomma et al., Deficiency in phytoalexin production causes enhanced susceptibility of Arabidopsis thaliana to the fungus Alternaria brassicicola, PLANT J, 19(2), 1999, pp. 163-171
Citations number
40
Categorie Soggetti
Plant Sciences","Animal & Plant Sciences
Journal title
PLANT JOURNAL
ISSN journal
09607412 → ACNP
Volume
19
Issue
2
Year of publication
1999
Pages
163 - 171
Database
ISI
SICI code
0960-7412(199907)19:2<163:DIPPCE>2.0.ZU;2-U
Abstract
The phytoalexin-deficient Arabidopsis mutant pad3-1, which is affected in t he production of the indole-type phytoalexin camalexin, has previously been shown not to display altered susceptibility to either the bacterium Pseudo monas syringae (Glazebrook and Ausubel, 1994; Proc. Natl. Acad. Sci. USA, 9 1: 8955-8959) or the biotrophic fungi Peronospora parasitica (Glazebrook et al., 1997; Genetics, 146: 381-392) and Erysiphe orontii (Reuber et al., 19 98; Plant J. 16: 473-485). We now show that this mutant is markedly more su sceptible than its wild-type parental line to infection by the necrotrophic fungus Alternaria brassicicola, but not to Botrytis cinerea. A strong cama lexin response was elicited in wild-type plants inoculated with either Alte rnaria brassicicola or Botrytis cinerea, whereas no camalexin could be dete cted in pad3-1 challenged with these fungi. Hence, PAD3 appears to be a key determinant in resistance to at least A. brassicicola. The induction of sa licylate-dependent and jasmonate/ethylene-dependent defense genes was not r educed in Alternaria-challenged pad3-1 plants compared to similarly treated wild-type plants. Camalexin production could not be triggered by exogenous application of either salicylate, ethylene or jasmonate and was not, or no t strongly, reduced in mutants with defects in perception of these defense- related signal molecules. Camalexin-production appears to be controlled by a pathway that exhibits little crosstalk with salicylate-, ethylene- and ja smonate-dependent signalling events.