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Title: Flagellin-induced immune responses in Arabidopsis thaliana
Author: Navarro, Lionel.
ISNI:       0000 0001 3440 0780
Awarding Body: University of East Anglia
Current Institution: University of East Anglia
Date of Award: 2005
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Plants and animals activate an innate immune response upon perception of pathogen-associated molecular patterns (PAMPs) such as bacterial flagellin. In Arabidopsis, flagellin perception elevates basal resistance to the virulent Pseudomonas syringae pv tomato DC3000 (Pto DC3000), although the molecular mechanisms involved remain elusive. We surveyed the early transcriptional response of Arabidopsis cell cultures and seedlings within 60 min of treatment with flg22, a peptide corresponding to the most conserved domain of flagellin. Using Affymetrix® microarrays, - 3.0% of 8200 genes displayed transcript level changes in flg22-elicited suspension cultures and seedlings. FLARE (FLAgellin Rapidly Elicited) genes mostly encode signalling components. We first compared FLARE gene sets and genes induced in different gene-forgene interactions. This analysis revealed a substantial overlap between FLARE genes and genes activated during bacterial and fungal race-specific defence responses. We also compared FLARE gene sets and genes induced in basal interaction upon bacterial treatments and infer that Pseudomonas syringae represses the flagellin-initiated defence response. We further performed a clustering of the FLARE genes and analysed their respective promoters for over-representation of cis-regulatory elements. A cluster of progressively up-regulated genes shared common regulatory motifs within their promoters. In contrast, no over-representation of regulatory motifs were identified within the promoter sets of repressed genes suggesting a potential posttranscriptional regulation of these genes. Accordingly, we found that flg22-induces a plant microRNA that causes degradation of mRNA for TIRl, an F-box auxin receptor. The resulting repression of auxin signalling restricts Pto DC3000 growth, implicating auxin in disease susceptibility, and miRNA-mediated suppression of auxin signalling in disease resistance. We next studied the molecular basis of flg22-induced growth inhibition of Arabidopsis elicited seedlings. We found that DELLA protein growth repressors, which are normally degraded upon gibberellin treatment, are stabilized by flg22 treatment. We also discover that DELLA proteins elevate resistance to A. brassicicola and inhibit basal resistance to Pto DC3000 through modification of the SA-JA/ET signal balance. This implicates GA-signalling in resistance to biotrophs and susceptibility to necrotrophs.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available