BSPP Presidential Meeting 2003

Plant Pathogen Genomics - From Sequence To Application

Genome sequencing and functional genomics of Erwinia carotovora subsp. atroseptica

Ian Toth1, Kenneth Bell1, Julian Parkhill2, Mohammed Sebaihia2, Leighton Pritchard1, Lizbeth Hyman1, and Paul Birch1

1 Scottish Crop Research Institute, Invergowrie, Dundee.
Pathogen Sequencing Unit, Wellcome Trust Sanger Research Institute, Cambridge.

Erwinia carotovora subsp. atroseptica (Eca) is an economically important pathogen of potato, causing blackleg of plants in the field and soft rot of tubers post-harvest. Its pathogenicity is primarily dependant on the tightly regulated production of large amounts of extra-cellular enzymes that degrade plant cell walls, with other factors such as iron acquisition and defence against the plant response also playing a role. In recent years, however, it has become clear that soft rot pathogenesis is more complex than previously thought and the relationship of Eca with potato and non-host plants is still far from being understood. To address these issues, the complete genome sequence and annotation of Eca has been determined at the Sanger Institute. Analysis of the genome has revealed a wealth of new information, including putative pathogenicity factors previously unknown in this organism. We are using computational analysis to determine as much as possible about these factors, and to compare the Eca genome sequence with those of other bacteria. Finally, a number of functional genomics programmes are being developed, including the use of micro-arrays, proteomics, mutation grids and improved bioassays to determine the role of target genes/regions in pathogenesis.

Signalling in the U. maydis/maize pathosystem: what we can learn from expression profiling

Regine Kahmann

Max Planck Institute for terrestrial Microbiology, Karl-von-Frisch-Strasse, D-35043 Marburg, Germany.

Ustilago maydis is the causative agent of corn smut disease. The pathogenic form is generated after mating of two compatible cells. Results from several laboraties have shown that the signalling pathways required for transmission of the pheromone signal during mating are also needed during pathogenesis. In particular, the components of a conserved MAP kinase module as well as tightly regulated cAMP signalling are needed for disease progression.Recent results suggest that these pathways have partially overlapping as well as distinct functions.

To analyze these pathways in more details we have performed a comparative transcriptome analysis using Affymetrix arrays that represent about 6200 of the estimated 7000 U. maydis genes. To this end we have generated strains in which the different signalling pathways can be activated genetically. We have then compared conditions where the MAP kinase Kpp2, the MAP kinase Kpp6 or the PKA Adr1 are active and have included pheromone-treated cells for comparison. I will present the results and then focus on a coregulated gene cluster involved in siderophore biosynthesis and iron uptake that came up as being differentially regulated by Adr1.

Genomic studies on the late blight pathogen, Phytophthora infestans

Paul R J Birch

Plant-Pathogen Interaction Programme, Scottish Crop Research Institute, Invergowrie, Dundee DD2 5DA, UK

Potato is the worlds fourth largest crop, global production of which is increasing at 4.5 % annually ( The most serious constraint to potato production is the oomycete pathogen Phytophthora infestans, cause of late blight. Resistance to P. infestans in wild or cultivated potato species can be either race-specific or non-race specific (field resistance). The hypersensitive response is implicated in all forms of resistance, whether host or non-host. An increasing number of genomic resources (including ESTs and BAC libraries) and functional genomic tools (such as microarrays, proteomics and viral vectors for expression of pathogen genes within the host or for silencing of endogenous host genes) are becoming available to study the mechanisms of pathogenicity in P. infestans and of resistance in potato. At SCRI, we are using some of these tools and resources to determine transcriptional changes at different stages of compatible and incompatible P. infestans-potato interactions. We are seeking candidate regulators and effectors of resistance, particularly involving the HR, in potato. We are also seeking, through forward genetics, association genetics and functional genomics, the avirulence genes in P. infestans that trigger resistance in the host.

Plant Virus Infections: Interactions between three genomes

Roger Hull

Department of Disease and Stress Biology, John Innes Centre, Norwich Research Park, Colney, Norwich NR4 7UH

The successful infection of a plant with a virus often requires the interaction of three genomes, those of the virus, the host and the arthropod or nematode vector. The understanding of these interactions is leading to new approaches to controlling viruses.

Viruses have genomes of either RNA or DNA, with most plant viruses having RNA genomes. The genome organizations of all but one of the 70 genera of plant viruses have now been determined. These genomes comprise a replicon, those genes required to replicate the viral nucleic acid, and various other gene cassettes that facilitate functions such as movement within a host plant and transmission from an infected to a healthy plant host.

The functions on the host plant genome that interact with the virus include those that the virus "highjacks" to enable its replication and those from defence genes. Similarly, plant functions that interact with the arthropod (or nematode) vector include attractants, both chemical attractant and colour, and those that protect the plant against pests.

Little is known about the detailed genomes of arthropod or nematode vectors of plant viruses. However, there must be genes that enable specific interactions with the viruses that they transmit and the host that they feed on or colonize.

Obviously the details of many of these interactions are complex and, in many cases, unknown. There are both positive and negative interactions between the virus and host and vector and host and successful virus infection is often a balance between attraction and defence. In this talk, I will give some examples of these interactions to illustrate the complexity and to identify specific situations that can be capitalized upon to effect control of important diseases.