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Bacterial disease resistance in Arabidopsis through flagellin perception



Plants and animals recognize microbial invaders by detecting pathogen-associated molecular patterns (PAMPs)1,2,3,4,5 such as flagellin6,7,8,9,10. However, the importance of flagellin perception for disease resistance has, until now, not been demonstrated7,8,9,10,11. Here we show that treatment of plants with flg22, a peptide representing the elicitor-active epitope of flagellin6, induces the expression of numerous defence-related genes and triggers resistance to pathogenic bacteria in wild-type plants, but not in plants carrying mutations in the flagellin receptor gene FLS2. This induced resistance seems to be independent of salicylic acid, jasmonic acid and ethylene signalling. Wild-type and fls2 mutants both display enhanced resistance when treated with crude bacterial extracts, even devoid of elicitor-active flagellin, indicating the existence of functional perception systems for PAMPs other than flagellin. Although fls2 mutant plants are as susceptible as the wild type when bacteria are infiltrated into leaves, they are more susceptible to the pathogen Pseudomonas syringae pv. tomato DC3000 when it is sprayed on the leaf surface. Thus, flagellin perception restricts bacterial invasion, probably at an early step, and contributes to the plant's disease resistance.

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We thank H. Angliker for help with the microarray procedure; R. Ulm and D. Chinchilla for critically reading the manuscript; C. Molteni and B. Thürig for technical help; the Nottingham Arabidopsis Stock Centre for etr1-3, ein2-1, jar1-1, pad2-1 and pad4-1 seeds; the Torrey Mesa Research Institute for the SAIL_691-C4 line; J. Parker for eds1-2, sgt1b-3 and rar1-13 seeds; W. Achouak for the Pseudomonas brassicacearum strain; S. Y. He for Pseudomonas syringae pv. tomato DC3000 HrpS- mutant strain; and N. Kraus and H. Sierotzky for the plant growing facilities. This work was supported by the Novartis Research Foundation, by the Gatsby Charitable Foundation and by a grant from the Swiss National Foundation.

Author information

Competing interests

The authors declare that they have no competing financial interests.

Correspondence to Thomas Boller.

Supplementary information

  1. Supplementary Methods

    Description of the microarray experiment in MIAME compliant format. (DOC 23 kb)

  2. Supplementary Figure 1

    Genome-wide analysis of flg22-dependent gene expression in Ler-0 and fls2-17 seedlings. (PDF 85 kb)

  3. Supplementary Figure 2

    A null fls2 mutation in the ecotype Col-0 leads to enhanced disease susceptibility. Wild-type Col-0 and fls2 null mutant plants were sprayed with 5x108 cfu/ml Pst DC3000, or water. Symptoms and number of bacteria were scored 4 dpi. (PPT 184 kb)

  4. Supplementary Figure 3

    Ws-0 plants transformed with FLS2p::FLS2-3xmyc regain flg22 responsiveness. The complemented line expressed the FLS2-3xmyc fusion protein and regained the capacity to undergo flg22-induced oxidative burst and seedling growth inhibition. (PPT 95 kb)

  5. Supplementary Table 1

    Flagellin-regulated genes. (XLS 529 kb)

  6. Supplementary Table 2

    Resistance and resistance-associated genes induced upon flg22 treatment. (XLS 29 kb)

  7. Supplementary Table 3

    Receptor-like kinases induced upon flg22 treatment. (XLS 41 kb)

  8. Supplementary Table 4

    Frequency of occurrence of conserved motifs for different types of transcription factors in the flg22-induced RLK promoters. (PDF 84 kb)

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Further reading

Figure 1: Treatment with flagellin limits Pst DC3000 growth.
Figure 2: Treatment with different bacterial extracts limits subsequent growth of Pst DC3000 in Ler-0 and fls2-17 plants.
Figure 3: Bacterial disease resistance is determined by flagellin perception.


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