Roles of plant hormone signalling components in plant defence and susceptibility
Lead Research Organisation:
University of East Anglia
Department Name: Sainsbury Laboratory
Abstract
For the Non Technical Summary, see the 'Revised objectives, costings, summary, technical summary ' document (uploaded 03/03/2006), under the 'Documents' tab.
Technical Summary
The elicitor bacterial flagellin (flg22) triggers reduced auxin sensitivity by inducing a microRNA (miR393) that targets an auxin receptor, TIR1. Overexpression of miR393 enhances bacterial resistance, and overexpression of a miR393-refractory paralog of TIR1 (AFB1) enhances disease. We will investigate how auxin promotes virulence, and how bacteria activate auxin signalling, by asking; 1- Do Arabidopsis mutants altered in auxin sensitivity or abundance show altered interactions with Pseudomonas syringae pv tomato DC3000 (PtoDC3000)? 2- Does altered auxin regulation affect sensitivity to other biotrophic and necrotrophic pathogens? 3- Does auxin affect defence responses such as the oxidative burst, callose deposition, kinase activation and ethylene (ET) and jasmonic acid (JA) synthesis and (using microarrays) differential gene regulation? 4- How does auxin promote bacterial disease sensitivity? (i) ARF transcription factors complex with AUX/IAA repressor proteins and bind to auxin-responsive promoters. There are 23 ARFs, for 18 of which T-DNA lines are available. We will test which ARF is involved in sensitivity to PtoDC3000 by examining mutants for enhanced resistance. (ii) Wild type and various auxin mutant leaves will be infiltrated with PtoDC3000 or PtoDC3000 hrcC mutants, and assayed over a detailed time course for defence gene expression. (iii) Auxin might activate JA signalling; we will measure JA levels and responses after auxin treatment, and test if bacterial sensitivity can be restored in 35S:miR393 lines by addition of JA. 5- PtoDC3000 does not make auxin; we will test if bacterial effector proteins trigger auxin signalling by comparing induction of auxin-responsive promoters to PtoDC3000 and to PtoDC3000 hrc mutants. 6- We will try to examine gene expression specifically in leaf L2 mesophyll cells by expressing a tagged ribosomal subunit using a Rubisco promoter, and affinity purifying polysomes with the tag for mRNA preparation.
Organisations
People |
ORCID iD |
| Jonathan Jones (Principal Investigator) |
Publications
Robert-Seilaniantz A
(2011)
The microRNA miR393 re-directs secondary metabolite biosynthesis away from camalexin and towards glucosinolates.
in The Plant journal : for cell and molecular biology
| Description | Plants are constantly under microbial attack, and plants respond using distinct and antagonistic pathways. Biotrophic pathogens keep the host alive during disease; plant defence responses are coordinated by salicylic acid (SA) and can lead to cell death. Necrotrophic pathogens grow on dead tissue; plant defence is controlled by jasmonic acid (JA) and ethylene (Et) signalling. Successful pathogens make effector molecules that interfere with the extent to which pathogen elicitors such as flagellin and chitin activate defence. In Arabidopsis, flagellin induces a small RNA (a microRNA- miR393) that targets for destruction the mRNA that encodes the receptor for the plant hormone auxin. Overexpression of miR393 made the plant more biotroph resistant, and overexpression of an auxin receptor mRNA that is refractory to miR393 more biotroph sensitive. The goal of part of this work was to understand how auxin promotes biotroph disease, and how reduced sensitivity to auxin enhances disease resistance. We tested the effect of auxin on different plant/pathogen interactions, and confirmed that high auxin signaling/content correlates with increased biotroph susceptibility. In contrast, weak auxin signaling is associated with increased resistance to biotrophs and increased susceptibility to necrotrophs. By measuring gene expression and hormone levels, we found that auxin blocks SA signaling, and that suppression of auxin signaling increases metabolic flow towards the indole glucosinolate (IG) pathway. IGs are antimicrobial compounds with activity against biotrophs. Auxin does not affect the JA pathway, so suppression of SA action by auxin is not due to increased JA but rather to an effect on SA signaling. We found that HopC1 from the phytopathogenic bacterium Pseudomonas syringae pv. tomato DC3000 (PstDC3000) is a bacterial effector that directly activates auxin signaling, and we continue to investigate the underlying mechanism. Gibberellin (GA) promotes plant growth by destabilizing DELLA regulatory proteins. We investigated the roles of GA and DELLA proteins in plant defence. We found that Arabidopsis mutants lacking DELLA proteins are susceptible to the fungal necrotrophs Alternaria brassicicola (A.b.) and Botrytis cinerea, but are more resistant to biotrophs PstDC3000 and downy mildew. della loss-of-function mutants show enhanced cell death and elevated SA levels compared to wild type (WT) plants inoculated with PstDC3000. mRNA expression profiling of Arabidopsis wild type and della mutant leaves in response to flagellin, Pst DC3000 and A.b. indicates that DELLA proteins negatively regulate expression of several genes involved in SA signaling and positively regulate expression of genes in JA/ET-signaling. DELLA proteins may thus promote susceptibility to virulent biotrophs and resistance to necrotrophs by altering the relative strength of SA- and JA/ET-signaling. Expression of several genes involved in the detoxification of reactive oxygen species (ROS), such as peroxidases and superoxide dismutases are decreased in della mutants compared to the WT plants. We also found increased accumulation of flg22-induced ROS in della mutants compared to WT plants. Addition of GA confers enhanced sensitivity to A. b. but increased resistance against Pst DC3000. Remarkably, addition of JA with GA enhances and does not relieve A.b. sensitivity. In contrast, pre-treatment with paclobutrazol, which inhibits GA biosynthesis, thus stabilizing DELLA proteins, enhanced resistance to A.b. Arabidopsis leaves pre-treated with GA, or GA plus JA, show decreased induction of genes involved in JA/ET- signaling and ROS detoxification compared to water pretreatment, and also accumulate increased levels of ROS compared to control plants. These results indicate that GA acts as a susceptibility factor for necrotrophs and plays roles in defence responses at least partly by regulating ROS detoxification in Arabidopsis. |
| Exploitation Route | Understanding hormonal priming of defence |
| Sectors | Agriculture, Food and Drink |
| URL | http://www.ncbi.nlm.nih.gov/pubmed/21457368 |
| Description | Our findings provided new insights into the influence of plant hormones on disease resistance or susceptibility, and vice versa |
| First Year Of Impact | 2009 |
| Sector | Agriculture, Food and Drink |
| Impact Types | Cultural |