Abstract
Summary Cultivar‐strain specificity in the wheat–Zymoseptoria tritici pathosystem determines the infection outcome and is controlled by resistance genes on the host side, many of which have been identified. On the pathogen side, however, the molecular determinants of specificity remain largely unknown.We used genetic mapping, targeted gene disruption and allele swapping to characterise the recognition of the new avirulence factor Avr3D1. We then combined population genetic and comparative genomic analyses to characterise the evolutionary trajectory of Avr3D1.Avr3D1 is specifically recognised by wheat cultivars harbouring the Stb7 resistance gene, triggering a strong defence response without preventing pathogen infection and reproduction. Avr3D1 resides in a cluster of putative effector genes located in a genome region populated by independent transposable element insertions. The gene was present in all 132 investigated strains and is highly polymorphic, with 30 different protein variants identified. We demonstrated that specific amino acid substitutions in Avr3D1 led to evasion of recognition.These results demonstrate that quantitative resistance and gene‐for‐gene interactions are not mutually exclusive. Localising avirulence genes in highly plastic genomic regions probably facilitates accelerated evolution that enables escape from recognition by resistance proteins.
Highlights
Regardless of whether they are mutualistic or parasitic, colonising microbes evolve a high degree of specialisation to recognise and infect their hosts and overcome host-inducible defences (van der Does & Rep, 2017)
We studied the evolutionary trajectory of Avr3D1 by combining population genetic and comparative genomic analyses involving 132 Z. tritici strains originating from four field populations on three continents as well as 11 strains of the closest known relatives of Z. tritici
We identified an avirulence gene that has a large effect on some wheat cultivars, additional factors must contribute to the differences in virulence between the two strains, because the density of pycnidia formed by the Avr3D1 knockout in the avirulent strain was still lower than the pycnidia density produced by the virulent strain
Summary
Regardless of whether they are mutualistic or parasitic, colonising microbes evolve a high degree of specialisation to recognise and infect their hosts and overcome host-inducible defences (van der Does & Rep, 2017). Effectors are beneficial for host colonisation, some are recognised by certain host genotypes, triggering an immune response (Jones & Dangl, 2006; Lo Presti et al, 2015) This interaction typically follows the gene-for-gene model, in which a so-called resistance protein recognises an effector, which is called an avirulence factor (Avr) (Flor, 1971; Jones & Dangl, 2006). A common assumption is that resistance/avirulence gene interactions confer complete resistance, whereas quantitative resistance, understood here as incomplete or partial resistance that allows some pathogen infection and reproduction, is based on different, race-nonspecific and avirulenceindependent mechanisms This paradigm originated from work on biotrophic pathogens, where avirulence recognition often leads to complete immunity via induction of a hypersensitive response (Cook et al, 2015; Niks et al, 2015). Avirulence factors leading to quantitative resistance have only rarely been described (Schirawski et al, 2010; Rietman et al, 2012)
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