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Abstract Detail

Plant Defense

Anderson (nee Barker), Claire [1].

Analysis of an auto-active Hcr9 disease resistance protein reveals residues responsible for activation, repression and enhancement of signalling activity.

The tomato Cf-9 gene confers resistance to races of the fungal leaf mould pathogen, Cladosporium fulvum, that express the Avr9 avirulence gene. Cf-9 belongs to a large family of Hcr9 genes that encode membrane-bound proteins with large extracellular leucine-rich repeat domains and short cytosolic tails. However, unlike many other disease resistance proteins, Hcr9 proteins lack any region that might be predicted to have a signaling function. Therefore, it is a challenge to understand how this class of resistance proteins function. Recently a lesion mimic tomato mutant was identified that possessed a novel gene arising from in-frame recombination between Cf-9 and the upstream paralogue, Hcr9-9A. The recombinant gene, named Hcr9-M205, encoded an auto-active resistance protein that caused chlorosis and the expression of PR-5 genes when transiently expressed in tobacco (Barker et al. (2006) Plant J. 46, 369-384). Further analysis of Hcr9-M205 through the generation of domain swaps between Cf-9 and Hcr9-9A has revealed key regions of the Hcr9-M205 protein that are required for auto-activity, including a single leucine-rich repeat motif that is sufficient and necessary for a basal level of defence activation to occur, a single amino acid that can completely repress the auto-activity of Hcr9-M205 and an enhancer region that is required for activation of a full-scale defence response. This analysis has provided new insight into the complex roles of the Hcr9 leucine-rich repeat domain during activation of the plant defence response.

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1 - CSIRO Plant Industry, GPO Box 350, Glen Osmond, SA, 5064, Australia

disease resistance protein
leucine-rich repeat.

Presentation Type: ASPB Minisymposium
Session: M09
Location: Continental A/Hilton
Date: Monday, July 9th, 2007
Time: 9:20 AM
Number: M09003
Abstract ID:642

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