Evaluating the importance of the tan spot ToxA–Tsn1 interaction in Australian wheat varieties

Abstract

The necrotrophic fungal pathogen Pyrenophora tritici‐repentis (Ptr) causes the major wheat disease tan spot, and produces multiple necrotrophic effectors that contribute to virulence. The proteinaceous effector ToxA induces necrosis in wheat genotypes possessing the Tsn1 gene, although the importance of the ToxA–Tsn1 interaction itself in varietal disease development has not been well studied. Here, 40 Australian spring wheat varieties were assessed for ToxA sensitivity and disease response to a race 1 wildtype Ptr isolate and ToxA‐deleted strain at both seedling and tillering growth stages. ToxA sensitivity was generally associated with disease susceptibility, but did not always predict spreading necrotic symptoms. Whilst the majority of Tsn1 varieties exhibited lower disease scores following toxa mutant infection, several exhibited no distinct differences between wildtype and toxa symptoms. This implies that ToxA is not the major determinant in tan spot disease development in some host backgrounds and indicates the presence of additional effectors. Unexpectedly, several tsn1 varieties exhibited a reduction in disease severity following toxa mutant inoculation, which may suggest an indirect role for ToxA in pathogen fitness. Additionally, increased chlorosis was observed following toxa mutant infection in three varieties, and further work is required to determine whether this is likely to be due to ToxA epistasis of ToxC symptoms. Taken together, these observations demonstrate that Ptr interacts with the host in a complex and intricate manner, leading to a variety of disease reactions that are dependent or independent of the ToxA–Tsn1 interaction.

Good Riddance? Breaking Disease Susceptibility in the Era of New Breeding Technologies

“…The presence of both, ToxA and ToxABP1, or the silencing of ToxABP1 in the absence of ToxA leads to similar necrotic phenotypes, indicating ToxA altering ToxABP1 function [65,66]. ToxA genetically interacts with the product of the toxin sensitivity gene Tsn1, which encodes a protein that resembles canonical Resistance proteins [9,67]. Functional TSN1 is involved in triggering ToxA-dependent cell death, which favors necrotrophic pathogen growth, and is thus a major S factor with agronomic relevance for both tan spot and leaf blotch in wheat [68].…”

Identification of quantitative trait loci conferring resistance to tan spot in a biparental population derived from two Nebraska hard red winter wheat cultivars

“…This suggests that the effect of these QTL is masked by that of the Ptr ToxA-Tsn1 interaction. Epitasis of the Ptr ToxA-Tsn1 interaction over other interactions has been reported in the wheat-Ptr system (Manning and Ciuffetti 2015;See et al 2018). As mentioned above, the effect of Ptr ToxA-Tsn1 interaction can be completely masked by the action of race-nonspecific resistance (Kariyawasam et al 2016).…”

“…However, new evidence has strongly suggested the existence of additional races (Ali et al 2010;Mereno et al 2015) as well as the presence of additional NEs in the current races (Friesen et al 2002;Moffat et al 2014). In addition, Ptr ToxA has been shown to have an epistatic effect on other unidentified NEs (Manning and Ciuffetti 2015;See et al 2018).…”

Genetic analysis of wheat sensitivity to the ToxB fungal effector from Pyrenophora tritici-repentis, the causal agent of tan spot

“…The role of ToxA as a key tan spot disease determinant has been demonstrated in interactions with many but not all wheat cultivars (Ciuffetti et al 1997). Recent work screening Australian wheat lines with a Ptr mutant carrying a deletion of ToxA has further highlighted the importance of ToxA in tan spot disease (See et al 2018). Disease levels were significantly reduced on about one third of the Tsn1 wheat lines.…”