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.
In response to disease, the plant defence response often involves a hypersensitive response (HR), visible as flecks of dead cells at sites of attempted entry. A continuously updated web page on plant pathology can be found at http://www.apsnet.org/
Plant diseases cause severe crop losses. Plant disease resistance (R) genes have been bred into crops from wild relatives of crop species. 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 is probably 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, our eventual aim is to clone enough R genes that we can mimic nature and deliver durable blight resistance by creating an R gene “polyculture”.
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).
Pathogens can’t avoid making certain molecules; for example, fungi make the cell wall component chitin, and bacteria make the motor 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 are mostly unknown.
Plants have evolved mechanisms to circumvent these effectors by recognizing them as cues to activate defence. R genes encode proteins that act as receptors for such effectors. To overcome an R gene, a pathogen must cease to produce the molecule the R protein detects; pathogens thus need a suite of effectors so that if one is resisted and must be discarded, others can substitute. These molecules are encoded by Avirulence genes (Avr genes), so-called because if they are functional, the pathogen will be avirulent on plants carrying the corresponding R gene.
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.
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. Arabidopsis carries ~56 RLPs, 4- 6 of which are involved in development, and the rest probably in resistance. Again, how these proteins signal is completely mysterious; much remains to be discovered.
