Jonathan Jones
Welcome
Plants and their pathogens and parasites have evolved together for millions of years. Examples of plant disease are widespread; in your garden, in fields, on your window-sill, or in the wild. Disease can result in rots, water-soaked lesions, blights, wilts, powdery or downy mildews, or rust lesions on the plant. Plant diseases can cause severe crop losses, that usual require control by agrichemicals. Notable current diseases are potato late blight, wheat rusts, soybean rust and Black Sigatoka of banana. A continuously updated web page on plant pathology can be found at http://www.apsnet.org/
In response to disease, plants activate defence mechanisms. Plant defence often involves a hypersensitive response (HR), visible as flecks of dead cells at sites of attempted entry. Plant disease resistance (R) genes have been bred into crops from wild relatives of crop species. Breeders are continually searching for new resistance genes and resistance gene combinations. However, by mutation or recombination, new races of the pathogen usually eventually appear that can overcome the R gene.
If R genes are so easily overcome, why has selection maintained them in wild species? This may be because wild plant populations are genetically heterogeneous, and unlike crops, are not planted as monocultures. Heterogeneity for disease resistance probably restricts pathogen epidemics in natural plant populations.
In our project to characterize natural variation for late blight resistance in wild potato species, we aim to clone multiple R genes that can be “stacked” to increase the prospects of delivering durable blight resistance.
Pathogens can’t avoid making certain molecules; for example, fungi make the cell wall component chitin, and bacteria make the flagellum protein flagellin. Plants have evolved the capacity to recognize such molecules, known as “Pathogen-associated molecular patterns (PAMPs)”. How then do successful pathogens still cause disease?
The answer lies in so-called effector molecules made by pathogens, which shut down the defence response elicited by PAMPs. Bacterial PAMPs and effectors are becoming well characterized, but those from fungi and oomycetes were mostly unknown. With the advent of new sequencing
Visualisation of capsidiol, a phytoalexin produced
during
the tobacco defense response, following
inoculation with
Phytophthora infestans
(right hand image shows leaf viewed
under UV light).methods, the genomes and thus the
effectoromes of all
plant pathogens are now “within range”.
There are two main classes of R genes, and a few other rarer classes.
The biggest class encodes cytoplasmic nucleotide binding, leucine rich repeat (NB-LRR) proteins that convert recognition of pathogen molecules to activation of defence mechanisms. How this works is currently a complete mystery, and thus a good problem to work on. This class of protein can confer resistance to nematodes, viruses, bacteria, fungi or oomycetes. NB-LRR proteins either have a TIR signalling domain at their N-termini, or they have a coiled coil domain. Genetic analysis has shown that these genes usually require the EDS1, PAD4, SGT1 and RAR1 genes for full functionality. We work on an interesting dual R gene system, both of which are required for effector recognition, and one of which carries a WRKY transcription factor domain. Another important class of R proteins carry extracellular LRRs, a transmembrane domain, and a short cytoplasmic domain. The tomato Cf-9 gene for leaf mould (Cladosporium fulvum) resistance was the first R gene to be identified encoding this so-called receptor-like protein (RLP) class, and activates defence mechanisms on exposure to the C. fulvum Avr9 peptide.
