Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 12/14/2006
Publication Date: 7/21/2007
Citation: Oliver, R.P., Solomon, P.S., Hane, J., Tan, K., Lowe, R., Waters, O., Stukenbrock, E.H., Mcdonald, B.A., Friesen, T.L. 2007. Fungal proteins, metabolites and signalling pathways controlling the interaction between wheat and Stagonospora nodorum. Meeting Abstract. XIII International Congress on Molecular Plant-Microbe Interactions, July 21-27, 2007, Sorrento, Italy.
Technical Abstract: We are analysing the wheat pathogen Stagonospora nodorum in order to determine the molecular basis of pathogenicity. The genome sequence of the wheat pathogen Stagonospora nodorum is the first Dothideomycete to be released. This taxon includes a large number of important plant pathogens. The sequence has facilitated experiments that have defined roles for the Ca2+/calmodulin, MAP kinase and cAMP-dependant signalling pathways and for the metabolites mannitol, arabitol, xylitol, malate, trehalose and aminolevulinate. Analysis of gene expression throughout infection points to three phases of nutrition; a lipolytic phase utilising internal stores; a glycolytic phase using external low molecular weight assimilates and hydrolytic phase using external polymerised substrates. The Dothideomycete group includes most or all pathogens that produce host-specific toxins. ToxA is produced by Pyrenophora tritici-repentis, the causal agent of tan spot in wheat and is responsible for virulence of the fungus on wheat genotypes carrying the dominant susceptibility gene Tsn1. A S. nodorum predicted gene, SnToxA is nearly identical to PtrToxA. Disruption of SnToxA significantly reduced disease on wheat lines carrying Tsn1. Sequencing of ToxA genes from a world wide collection of isolates of P. tritici-repentis and S. nodorum showed that all the P. tritici-repentis sequences were identical but that the S. nodorum sequences were highly variable. This pattern is strong evidence of horizontal gene transfer from S. nodorum to P. tritici-repentis. Furthermore, comparison of the sequences showed an excess of non-synonymous codon changes over synonymous, suggesting diversifying selection. This is expected of a protein that interacts directly and significantly with the product of Tsn1. P. tritici-repentis is a recently emerged disease and we suggest this emergence is linked to the acquisition of ToxA, prior to 1941, that enabled the rapid spread around the world. SnToxA is one of several toxins produced by S. nodorum. These studies raises several important and new problems. These include the effect of toxin possession and expression on the fecundity and survival of fungal strains carrying the toxins, the history of the possession and expression of toxin receptor genes in the host wheat and the mechanisms of sequence diversification in toxin genes. Progress in these areas will be described.