Host-specific toxins: effectors of necrotrophic pathogenicity

Abstract

SummaryHost-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.

Analysis of Two in Planta Expressed LysM Effector Homologs from the FungusMycosphaerella graminicolaReveals Novel Functional Properties and Varying Contributions to Virulence on Wheat

“…ETI frequently conforms to a gene-for gene model (Flor, 1971) whereby single genes/loci in the pathogen interact with single dominant genes/loci in the plant, giving rise to immunity. In contrast, an inverse model of the gene-for-gene system also exists that involves the interaction between individual effector genes from the pathogen and single dominant susceptibility loci in the plant (Friesen et al, 2008). In the latter scenario, the net result is to promote plant infection through the activation of plant cell death signaling pathways often resembling those triggered during ETI (Wolpert et al, 2002).…”

“…In the latter scenario, the net result is to promote plant infection through the activation of plant cell death signaling pathways often resembling those triggered during ETI (Wolpert et al, 2002). These mechanisms, described as effectortriggered susceptibility (Friesen et al, 2008), have been shown to favor plant infection by various necrotrophic fungi, and in particular two wheat (Triticum aestivum)-infecting fungi, Stagonospora nodorum and Pyrenophora tritici repentis (Friesen et al, 2006;Liu et al, 2009), which are the causal agents of leaf blotch and tan spot diseases, respectively.…”

“…One hypothesis is that that these pathogens might deploy specialized effectors (frequently but not always proteins) during particular phases of plant infection that facilitate their particular nutritional and reproductive lifestyle. These effectors could act either as infection phase-specific suppressors of plant defense responses or alternatively as activators, depending on the lifestyle of the fungus (Friesen et al, 2008;Solomon and Rathjen, 2010;de Jonge et al, 2011;Deller et al, 2011).…”

Plant breeding for disease resistance in the age of effectors

“…Foliar biotrophic pathogens pose serious challenges, but these are outweighed by the difficulty in assessing disease to necrotrophic foliar pathogens such as those caused by Dothideomycete fungi (Friesen et al 2008a) and even more so to pathogens of the stem, crown and root caused by genera such as Fusarium, Verticillium and Rhizoctonia. Many of these pathogens are now known to exist in a myriad of races, further adding to the difficulty.…”

“…In recent years the confusing term avirulence has been dropped and replaced by the neutral term "effector" (Kjemtrup et al 2000). Effectors also include so-called PAMPs (pathogen-associated molecular patterns; Nürnberger and Brunner 2002), host-specific toxin molecules (typically produced by fungi in the Pleosporales, Friesen et al 2008a), and non-specific toxins produced by many (all perhaps except the haustorial biotrophic) pathogens. It is also 15 years since the first resistance gene was cloned and together with several hundred R-genes we also have uncovered details of PAMP receptors, guard proteins and defence response pathway genes (Jones et al 1994;SchulzeLefert 2004;Shirasu et al 1999;Staskawicz et al 1984;Staskawicz et al 1995).…”