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Plants in which the RKS1 allele is over-expressed have an increased resistance to black rot disease

INRA’s researchers showed that RKS1 is a quantitative resistance gene conferring a broad spectrum resistance to several Xanthomonas campestris races and pathovars. This resistance mechanism in plants is associated with RKS1 expression regulation, and RKS1 allelic variation is a major component of quantitative resistance to Xc at the species level.

Figure: Phenotype of resistant (Col-0) and susceptible (Kas-1) accessions of A. thaliana; symptoms 7 days post-inoculation with Xcc568.. © INRA
Updated on 11/14/2013
Published on 10/29/2013

Black rot disease is still possibly the most important disease of vegetable Brassica (cabbage, cauliflower, broccoli, turnip, etc.) and related crops (rapeseed, canola, mustard, etc.). It is caused by Xanthomonas campestris pv. campestris (Xcc), a devastating worldwide bacterial vascular pathogen that can spread rapidly, resulting in yield losses that may exceed 50%.

INRA’s researchers steered by Dominique Roby have inoculated several natural accessions of Arabidopsis thaliana with the Xcc strain 568 pathogen and observed that plants exhibited contrasting resistance phenotypes: some were resistant to infection (Col-5), while others were more susceptible (Kas-1). They carried out QTL analysis and revealed that one major locus at chromosome 3, QRX3 (Quantitative Resistance to Xcc568), contributes to Xcc568 resistance. Among the predicted ORFs present at this locus, the researchers identified by phenotyping all the ko mutants available in this region a particular RKS1 allele as responsible for the resistant phenotype in Col-5 ecotype. The role of this allele was confirmed (i) in heterogeneous inbred lines, (ii) by silencing RKS1 expression in resistant plants, and (iii) by complementation of naturally susceptible plants with the RKS1 resistant allele. RKS1 (Resistance-related kinaSe 1) encodes an atypical serine-threonine kinase which may be part of a still puzzling plant defense pathway as this type of kinase has been described as important regulators of signaling networks. RKS1 is highly expressed in leaves of resistant plants (Col-5 and derived plants), while its transcripts are barely detectable in leaves of susceptible ones (Kas-1 and derived plants), which could explain the phenotype variation. At the same time, leaf infection by Xcc did not lead to any significant change in RKS1 expression. Moreover, researchers demonstrated that the RKS1-conferred resistance is effective against a broad spectrum of races of Xcc strains and other pathovars of X. campestris. A Genome Wide Association mapping approach confirmed that RKS1 is also a major component of quantitative resistance to Xcc568 at the species level, with again a significant association between variation in resistance among natural accessions and RKS1 expression. The signature of balancing selection acting on RKS1 indicates that a durable broad-spectrum resistance to Xc may be achieved in natural populations of A. thaliana

This innovation deals with a method for improving Brassica plant resistance to the black rot disease agent, as well as plants of the Solanaceae or Cucurbitaceae family, wherein the expression of the RKS1 resistant allele is increased. This provides new tools for plant breeders:

  • Diagnostic methods for selecting resistant plants
  • Diagnostic methods using the RKS1 allele as a DNA marker tightly linked to the locus controlling quantitative disease resistance for marker-assisted selection to incorporate these valuable traits
  • Introgression of the RKS1 resistant allele into chosen elite lines
  • Production of transgenic resistant plants

INRA Transfert is seeking partners of the plant breeding industry to further develop the patent filed by INRA (WO2013/110781), through licence or licence option with a R&D programme.

Scientific contact(s):

  • Dominique ROBY Plant-Microorganism Interactions Laboratory
INRA Transfert’s licensing-out officer:
Alice AGASSE (+33 1 42 75 93 54)


  • Carine Huard-Chauveau et al., PLOS Genetics, Sept 2013, Vol 9, Issue 9, e1003766