Host-specific toxins: effectors of necrotrophic pathogenicity
Article first published online: 1 APR 2008
Journal compilation © 2008 Blackwell Publishing Ltd. No claim to original US government works
Volume 10, Issue 7, pages 1421–1428, July 2008
How to Cite
Friesen, T. L., Faris, J. D., Solomon, P. S. and Oliver, R. P. (2008), Host-specific toxins: effectors of necrotrophic pathogenicity. Cellular Microbiology, 10: 1421–1428. doi: 10.1111/j.1462-5822.2008.01153.x
- Issue published online: 1 APR 2008
- Article first published online: 1 APR 2008
- Received 13 February, 2008; revised 17 March, 2008; accepted 20 March, 2008.
Host-specific toxins (HSTs) are defined as pathogen effectors that induce toxicity and promote disease only in the host species and only in genotypes of that host expressing a specific and often dominant susceptibility gene. They are a feature of a small but well-studied group of fungal plant pathogens. Classical HST pathogens include species of Cochliobolus, Alternaria and Pyrenophora. Recent studies have shown that Stagonospora nodorum produces at least four separate HSTs that interact with four of the many quantitative resistance loci found in the host, wheat. Rationalization of fungal phylogenetics has placed these pathogens in the Pleosporales order of the class Dothideomycetes. It is possible that all HST pathogens lie in this order. Strong evidence of the recent lateral gene transfer of the ToxA gene from S. nodorum to Pyrenophora tritici-repentis has been obtained. Hallmarks of lateral gene transfer are present for all the studied HST genes although definitive proof is lacking. We therefore suggest that the Pleosporales pathogens may have a conserved propensity to acquire HST genes by lateral transfer.