ARS | Publication request: Interspecific transfer of host-specific toxin genes in Stagonospora nodorum

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: December 14, 2006
Publication Date: March 20, 2007
Citation: Oliver, R.P., Solomon, P.S., Hane, J., Stukenbrock, E.H., Mcdonald, B.A., Liu, Z., Faris, J.D., Friesen, T.L. 2007. Interspecific transfer of host-specific toxin genes in Stagonospora nodorum. Meeting Abstract. 24th Fungal Genetics Conference. p. 61.

Technical Abstract: The proteinaceous host-specific toxin ToxA, produced by Pyrenophora tritici-repentis, confers virulence of the fungus on wheat genotypes carrying the dominant susceptibility gene Tsn1. Sensitivity to the purified toxin and susceptibility to the disease co-locates to the locus, Tsn1. A Stagonospora (Phaeosphaeria) nodorum predicted gene, SnToxA is nearly identical to PtrToxA. Disruption of SnToxA significantly reduced disease on wheat lines carrying Tsn1. Conversely, expression in strains lacking ToxA conferred virulence on Tsn1 wheat. Sequencing of ToxA genes from a world wide collection of isolates of P. tritici-repentis and S. nodorum and showed that all the P. tritici-repentis sequences were identical to each other. In contrast, the S. nodorum sequences were highly variable. P. tritici-repentis was first identified in 1902 but it was not until 1941 that typical tan spot symptoms were first described. Nowadays, P. tritici-repentis is a regular and abundant pathogen. Our evidence strongly suggests that ToxA was horizontally transferred to P. tritici-repentis some time prior to 1941. These new forms appear to have rapidly spread around the world, probably in grain shipments. Our work indicates that S. nodorum produces several other toxins. The presence of multiple host-specific toxins and their transfer between species raises many interesting evolutionary questions 1. How does toxin possession and expression affect the fecundity and survival of fungal strains? 2. How can we explain the possession and expression of toxin receptor genes in the host? 3. What are the mechanisms of sequence diversification in toxin genes? Recent experiments to address these issues will be described.