Award details

Isolation and characterisation of pathogenicity genes

Reference	BBS/E/C/00004186
Principal Investigator / Supervisor	Professor John Lucas
Co-Investigators / Co-Supervisors	Dr Paul Bowyer
Institution	Rothamsted Research
Department	Rothamsted Research Department
Funding type	Research
Value (£)	631,224
Status	Completed
Type	Institute Project
Start date	01/04/1999
End date	31/03/2004
Duration	60 months

Abstract

Fungi are damaging agents of plant disease world-wide. Many fungal plant pathogens initiate disease by forming specialised infection structures (appressoria) on the surface of the host plant. Inhibition of infection structure formation is an effective means of controlling disease, as shown by anti-penetrant fungicides such as tricyclazole. Understanding the factors controlling induction and formation of infection structures will provide novel targets for fungicide development. Tapesia yallundae causes eyespot disease of cereals. This fungus elaborates two distinct types of infection structure; the first is a simple appressorium required for penetration of the coleoptile. The second is a multicellular infection cushion (or plaque), which acts as a compound appressorium. This is required for penetration of mature leaf sheaths at later stages of infection, leading to damaging lesions. We have established an in vitro system for induction of infection plaque formation. The key trigger for plaque development is mechanical pressure rather than thigmotropism. Preliminary investigations show that, unlike other pathogens, cAMP strongly represses plaque formation. Studies using chemical inhibitors of signal transduction components also suggest the involvement of pertussis sensitive G-proteins and adenylate cyclase. Project objectives: 1) Characterisation of the signal inducing infection structure formation in the eyespot fungus. Cloning of the receptor or sensor component. 2) Cloning and characterisation of genes involved in signal transduction in this pathogen. 3) Use of reporter genes to screen for mutants deficient in reorganisation of the cytoskeleton during infection structure formation. 4) Isolation of chemically generated mutants which are unable to respond to mechanical stress or which can form infection structures without stimulus.

Summary

unavailable

Committee	Closed Committee - Plant & Microbial Sciences (PMS)
Research Topics	X – not assigned to a current Research Topic
Research Priority	X – Research Priority information not available
Research Initiative	X - not in an Initiative
Funding Scheme	X – not Funded via a specific Funding Scheme

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