The University of Edinburgh 2009
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RESEARCH PROGRAMMES
Gene discovery via gain-of-function genetics 
A large proportion of genes in the Arabidopsis thaliana, Drosophila melanogastor, Caenorhabditis elegans and Saccharomyces cerevisiae genomes have no obvious loss-of-funct ion phenotype (Tani et al. 2004). This phenomenon can be explained by two mechanisms of compensat ion. The first is the presence of duplicate genes, where loss-of-funct ion in one copy can be compensated by the other copy or copies. The second mechanism of compensat ion stems from the existence of alternat ive metabolic pathways and regulatory networks.. 

Role of ROIs, RNIs and cognate redox signalling in the establishment of plant disease resistance 
One of the most rapid defense responses engaged following pathogen recognition is the so-called oxidative burst, which constitutes the production of reactive oxygen intermediates (ROIs), primarily superoxide (O2 -) and hydrogen peroxide (H2O2), at the site of attempted invasion (Grant and Loake, 2000). In addition, nitric oxide (NO), a key signal molecule in the animal immune, nervous and vascular systems, has also been shown to accumulate during HR formation...

Determining the molecular basis of resistance and susceptibility of Arabidopsis towards necrotrophic pathogens
While there has been significant recent progress in determining the genetic basis of race- specific disease resistance, the nature of plant responses against necrotrophic pathogens remain relatively unexplored. To help address this deficiency, we are investigating the interaction of Arabidopsis with the necrotrophic pathogen Botrytis cinerea. We have identified a series of novel Arabidopsis mutants that express either increased resistance or enhanced susceptibility against B. cinerea. 

Genetic basis of non-host disease resistance 
Plant immunity against the majority of microbial pathogens is conveyed by a phenomenon known as non-host resistance (NHR) (Heath, 2000). This defence mechanism affords durable protection to plant species against given species of pathogens. This contrasts with the well-studied host resistance, mediated by the products of plant resistance (R) genes, which establish pathogen race- or cultivar-specific resistance... 

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