The rise of necrotrophic effectors

Abstract

Many biotrophic pathogens, which require living plant tissues for colonization, interact with their hosts in a gene-for-gene (GFG) manner whereby plant disease resistance (R) genes recognize products of specific avirulence (Avr) genes in pathogens leading to disease resistance (Flor, 1956). In these interactions, the absence of either the R gene, or the corresponding Avr gene results in disease. GFG interactions have also been well documented in the pathosystem involving the necrotrophic fungal pathogen Parastagonospora nodorum (also known as Septoria, Stagonospora, Leptosphaeria and Phaeosphaeria nodorum) and wheat. However, in this case, the interactions lead to increased disease when Parastagonospora nodorum expresses specific necrotrophic effector (NE) genes and wheat contains the corresponding dominant sensitivity genes. This type of interaction is often described as an 'inverse' GFG (Fig. 1).

A framework for community curation of interspecies interactions literature

“…Curating experiments with a gene-for-gene relationship For a gene-for-gene pathogen-host interaction type (when a known genetic interaction is conferred by a specific pathogen avirulence gene product and its cognate host resistance gene product) (Figure 2c, d, further described in the figure legend) (Flor, 1956;Jones & Dangl, 2006;Kanyuka, Igna, Solomon, & Oliver, 2022) the 'gene-for-gene phenotype' metagenotype workflow is followed. The metagenotypes and phenotype annotations are made in the same way as the standard 'pathogen-host interaction phenotype' workflow, but with different supporting data.…”

Chromatin-immunoprecipitation reveals the PnPf2 transcriptional network controlling effector-mediated virulence in a fungal pathogen of wheat

“…The Parastagonospora nodorum -wheat interaction has become a model fungal-plant pathosystem to study the molecular virulence factors underpinning infection. The fungus produces small secreted effector proteins that selectively interact with host-receptors encoded by dominant susceptibility-genes (1, 2). These interactions occur in a gene-for-gene manner that causes ‘effector-triggered susceptibility’ in the host plant, quantitatively affecting the disease which manifests as septoria nodorum blotch.…”