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Journal article

Characterization of Arabidopsis enhanced disease susceptibility mutants that are affected in systemically induced resistance

  • Ton, Jurriaan Graduate School Experimental Plant Sciences, Section of Phytopathology, Faculty of Biology, Utrecht University, the Netherlands - Laboratoire de Biochimie, NCCR, Universiteé de Neuchâtel, Switzerland
  • Vos, Martin De Graduate School Experimental Plant Sciences, Section of Phytopathology, Faculty of Biology, Utrecht University, the Netherlands
  • Robben, Charlotte Graduate School Experimental Plant Sciences, Section of Phytopathology, Faculty of Biology, Utrecht University, the Netherlands
  • Buchala, Antony J. Department of Biology, University of Fribourg, Switzerland
  • Métraux, Jean-Pierre Department of Biology, University of Fribourg, Switzerland
  • Loon, L. C. Van Graduate School Experimental Plant Sciences, Section of Phytopathology, Faculty of Biology, Utrecht University, the Netherlands
  • Pieterse, Corné M. J. Graduate School Experimental Plant Sciences, Section of Phytopathology, Faculty of Biology, Utrecht University, the Netherlands
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    2002
Published in:
  • The Plant Journal. - 2002, vol. 29, no. 1, p. 11-21
Defence signalling
ISR
Jasmonic acid
Ethylene
Salicylic acid
SAR
English In Arabidopsis, the rhizobacterial strain Pseudomonas fluorescens WCS417r triggers jasmonate (JA)- and ethylene (ET)-dependent induced systemic resistance (ISR) that is effective against different pathogens. Arabidopsis genotypes unable to express rhizobacteria-mediated ISR against the bacterial pathogen Pseudomonas syringae pv. tomato DC3000 (Pst DC3000) exhibit enhanced disease susceptibility towards this pathogen. To identify novel components controlling induced resistance, we tested 11 Arabidopsis mutants with enhanced disease susceptibility (eds) to pathogenic P. syringae bacteria for WCS417r-mediated ISR and pathogen-induced systemic acquired resistance (SAR). Mutants eds4-1, eds8-1 and eds10-1 failed to develop WCS417r-mediated ISR, while mutants eds5-1 and eds12-1 failed to express pathogen-induced SAR. Whereas eds5-1 is known to be blocked in salicylic acid (SA) biosynthesis, analysis of eds12-1 revealed that its impaired SAR response is caused by reduced sensitivity to this molecule. Analysis of the ISR-impaired eds mutants revealed that they are non-responsive to induction of resistance by methyl jasmonate (MeJA) (eds4-1, eds8-1 and eds10-1), or the ET precursor 1-aminocyclopropane-1-carboxylate (ACC) (eds4-1 and eds10-1). Moreover, eds4-1 and eds8-1 showed reduced expression of the plant defensin gene PDF1.2 after MeJA and ACC treatment, which was associated with reduced sensitivity to either ET (eds4-1) or MeJA (eds8-1). Although blocked in WCS417r-, MeJA- and ACC-induced ISR, eds10-1 behaved normally for several other responses to MeJA or ACC. The results indicate that EDS12 is required for SAR and acts downstream of SA, whereas EDS4, EDS8 and EDS10 are required for ISR acting either in JA signalling (EDS8), ET signalling (EDS4), or downstream JA and ET signalling (EDS10) in the ISR pathway.
Faculty
Faculté des sciences et de médecine
Department
Département de Biologie
Language
  • English
Classification
Biological sciences
License
License undefined
Identifiers
Persistent URL
https://folia.unifr.ch/unifr/documents/300004
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