Effector-triggered defence against apoplastic fungal pathogens

Stotz, Henrik U.; Mitrousia, Georgia; Wit, P.J.G.M. de; Fitt, Bruce D.L.

doi:10.1016/j.tplants.2014.04.009

Cited by 172 publications

(166 citation statements)

References 80 publications

(115 reference statements)

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“…We hypothesise that the magnitude of the defence response is not strong enough to prevent the progression of the infection and/or that the downregulation of Avr3D1 during the necrotrophic phase substantially decreases the defence response. The induction of this type of partial resistance might be a shared characteristic among nonobligate pathogens that grow in the apoplast and normally do not trigger a hypersensitive response (Stotz et al ., 2014). The strength of this partial or incomplete resistance response may still be sufficient to limit propagation of the pathogen under field conditions, in which case the underlying resistance gene could be a valuable source of resistance for breeding programmes.…”

Section: Discussionmentioning

confidence: 99%

A fungal avirulence factor encoded in a highly plastic genomic region triggers partial resistance to septoria tritici blotch

et al. 2018

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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.

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Section: Discussionmentioning

confidence: 99%

A fungal avirulence factor encoded in a highly plastic genomic region triggers partial resistance to septoria tritici blotch

et al. 2018

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“…Recently, to explain interactions between fungal pathogens and their host plants, Stotz et al . (2014) summarized another defence mechanism termed effector‐triggered defence (ETD). Compared with ETI, ETD responses against pathogens are relatively slow and not associated with a fast hypersensitive cell death response in hosts (Boys et al ., 2012; Bozkurt et al ., 2012; Jones and Dangl, 2006; Stotz et al ., 2014; Thirugnanasambandam et al ., 2011; Valent and Chang, 2010).…”

Section: Introductionmentioning

confidence: 99%

The wheat NB‐LRR gene TaRCR1 is required for host defence response to the necrotrophic fungal pathogen Rhizoctonia cerealis

Zhu

et al. 2017

Plant Biotechnology Journal

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SummaryThe necrotrophic fungus Rhizoctonia cerealis is the major pathogen causing sharp eyespot disease in wheat (Triticum aestivum). Nucleotide‐binding leucine‐rich repeat (NB‐LRR) proteins often mediate plant disease resistance to biotrophic pathogens. Little is known about the role of NB‐LRR genes involved in wheat response to R. cerealis. In this study, a wheat NB‐LRR gene, named TaRCR1, was identified in response to R. cerealis infection using Artificial Neural Network analysis based on comparative transcriptomics and its defence role was characterized. The transcriptional level of TaRCR1 was enhanced after R. cerealis inoculation and associated with the resistance level of wheat. TaRCR1 was located on wheat chromosome 3BS and encoded an NB‐LRR protein that was consisting of a coiled‐coil domain, an NB‐ARC domain and 13 imperfect leucine‐rich repeats. TaRCR1 was localized in both the cytoplasm and the nucleus. Silencing of TaRCR1 impaired wheat resistance to R. cerealis, whereas TaRCR1 overexpression significantly increased the resistance in transgenic wheat. TaRCR1 regulated certain reactive oxygen species (ROS)‐scavenging and production, and defence‐related genes, and peroxidase activity. Furthermore, H2O2 pretreatment for 12‐h elevated expression levels of TaRCR1 and the above defence‐related genes, whereas treatment with a peroxidase inhibitor for 12 h reduced the resistance of TaRCR1‐overexpressing transgenic plants and expression levels of these defence‐related genes. Taken together, TaRCR1 positively contributes to defence response to R. cerealis through maintaining ROS homoeostasis and regulating the expression of defence‐related genes.

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“…It is defined as the immune response that is generated in host plants upon recognition of a pathogen Avr gene by the plant R gene (Stuart et al, 2013) and is also known as a direct interaction. When the pathogen first infects the host, Pathogen Associated Molecular Patterns (PAMP)-triggered immunity (PTI) is initiated as plant pattern recognition receptors (PRRs) recognise PAMPs extracellularly (Stotz et al, 2014). In plants that are resistant to the pathogen, ETI is triggered leading to a hypersensitive response often causing localised cell death (Stotz et al, 2014).…”

Section: Effector Triggered Immunitymentioning

confidence: 99%

“…When the pathogen first infects the host, Pathogen Associated Molecular Patterns (PAMP)-triggered immunity (PTI) is initiated as plant pattern recognition receptors (PRRs) recognise PAMPs extracellularly (Stotz et al, 2014). In plants that are resistant to the pathogen, ETI is triggered leading to a hypersensitive response often causing localised cell death (Stotz et al, 2014). Stotz et al (2014) also classify immune response in apoplastic leaf pathogens like Cladosporum fulvum, Zymoseptoria tritici and L. maculans under the broader term of effector triggered defence (ETD).…”

Section: Effector Triggered Immunitymentioning

confidence: 99%

“…In plants that are resistant to the pathogen, ETI is triggered leading to a hypersensitive response often causing localised cell death (Stotz et al, 2014). Stotz et al (2014) also classify immune response in apoplastic leaf pathogens like Cladosporum fulvum, Zymoseptoria tritici and L. maculans under the broader term of effector triggered defence (ETD). Effectors can be recognised directly and indirectly (Stuart et al, 2013).…”

Section: Effector Triggered Immunitymentioning

confidence: 99%

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Population diversity and genomics of the fungal pathogen of canola Leptosphaeria maculans

Patel¹

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Canola (Brassica napus) is an important agricultural crop in Australia. Its value as an agricultural commodity has dramatically increased over the past few years to >$2000 million (AUD) in 2015.However, the production of this prosperous crop is threatened by up to 34 different pests, including fungal, bacterial and viral pathogens. Diseases caused by these pathogens lead to substantial crop losses that collectively amount to $130 million (AUD) each year. Leptosphaeria maculans (blackleg) is a ubiquitous ascomycete fungus that is the major causal agent of disease on canola plants. It is called blackleg due to its necrotrophic effects that cause stem canker at the base of the stem during the last stages of infection. When canola was first introduced to Australia as an agricultural crop in the 1970s, blackleg disease led to almost 90% crop losses, threatening to drive the nascent canola industry in Australia to the ground. In recent years, crop losses still amount to $76.6 million (AUD) per annum. Therefore, it is imperative to devise methods to control the devastating effects of this pathogen to protect this economically significant crop. In order to do so, we must decipher the genomic content that drives this pathogen to cause large-scale infections in the field.Blackleg disease is a major concern not only in Australia, but also in other parts of the world such as Europe and Canada. Over the past few years, scientists have made significant advances in decoding the genome of this pathogen. It has been established that L. maculans interacts in a genefor-gene manner with its host. It is composed of disease-causing avirulence (Avr) genes that are specifically recognised by the corresponding resistance (R) gene in the host plant. The specific location and characterisation of the Avr genes AvrLm1, AvrLm6, AvrLm4-7, AvrLm11, AvrLmJ1, AvrLm2 and AvrLm3 has been determined. Furthermore, the reference genome for this pathogen was sequenced in 2011. The reference genome based on the strain v23.1.3 is 45.12 Mb and is scaffolded onto 76 supercontigs. It was reported to be bipartite in nature, composed of AT and GCrich blocks and riddled with truncated copies of transposable elements (TEs) that were affected by Repeat-Induced Point (RIP) mutations. The availability of a reference genome has greatly assisted in designing bioinformatics tools to analyse the genomic content of this pathogen. Here we contribute to the growing pool of knowledge of blackleg genomics.This thesis begins by shedding light on the population diversity of this pathogen in Australia. We used Single Nucleotide Polymorphisms (SNPs) and sampled a large variety of isolates from different canola-growing regions across Australia. We were able to conclude that the Australian blackleg population is panmictic in nature, where members of the population interact randomly with one another, leading to high diversity via sexual reproduction. Increased genetic diversity amongst the population contributes significantly to increase the evolutionary potential of thi...

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Effector-triggered defence against apoplastic fungal pathogens

Abstract: HighlightsETD is triggered by RLPs that engage the receptor-like kinase SOBIR1.ETD triggers cell wall-related defence responses.ETD does not eliminate apoplastic pathogens.

Cited by 172 publications

References 80 publications

A fungal avirulence factor encoded in a highly plastic genomic region triggers partial resistance to septoria tritici blotch

A fungal avirulence factor encoded in a highly plastic genomic region triggers partial resistance to septoria tritici blotch

The wheat NB‐LRR gene TaRCR1 is required for host defence response to the necrotrophic fungal pathogen Rhizoctonia cerealis

Population diversity and genomics of the fungal pathogen of canola Leptosphaeria maculans

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