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Dernière mise à jour : Mai 2018

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Institut Sophia Agrobiotech

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Corruption of ABA signaling favors oomycete diseases

Corruption of ABA signaling favors oomycete diseases. (IPO Team)

To decipher the mechanisms that govern successful infection, we use Arabidopsis thaliana as model host for the leaf-infecting biotrophic Hyaloperonospora arabidopsidis (Hpa). Analysis of the A. thaliana transcriptome upon interaction with Hpa revealed a set of genes upregulated during all stages of infection. One of theses genes codes for a receptor-like protein kinase, which harbors an extracellular malectin-like domain in addition to leucine-rich repeats. We showed this gene being an ancestor of successive duplications that gave rise to a cluster of 11 genes, coding for highly similar proteins. We called it Impaired Oomycete Susceptibility 1 (IOS1), as a knock-out mutant showed strongly diminished disease progression upon infection with Hpa and Phytophthora parasitica. Further analyses revealed that the mutant was also less suceptible to infection by the biotrophic fungus, Erysiphe crucifererum, but not to bacterial pathogens, thus indicating a role for disease established by filamentous (hemi-)biotrophs. We found that IOS1 negatively regulates ABA signaling in Arabidopsis, and that oomycetes activate transcription of this receptor gene to attenuate the hormone signaling pathway during infection.

Hpa-infection represses ABA signaling, as monitored by reporter gene expression driven by the ABA-sensitive promoter RD29B. This repression is derepressed in the ios1-1 mutant showing that the Hpa-responsive ABA downregulation proceeds through IOS1

Hpa-infection represses ABA signaling, as monitored by reporter gene expression driven by the ABA-sensitive promoter RD29B. This repression is derepressed in the ios1-1 mutant showing that the Hpa-responsive ABA downregulation proceeds through IOS1

  • Hok S, Danchin EG, Allasia V, Panabières F, Attard A, Keller H. (2011) An Arabidopsis (malectin-like) leucine-rich repeat receptor-like kinase contributes to downy mildew disease. Plant Cell  and Environment34: 1944-1957