Multiple strategies for pathogen perception by plant immune receptors

Césari, Stella

doi:10.1111/nph.14877

Cited by 214 publications

(213 citation statements)

References 43 publications

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“…In the arms race between plants and microbial plant pathogens, plants develop complex and multilayered immune systems for self‐defence: pathogen‐ or microbe‐associated molecular patterns (PAMPs/MAMPs)‐triggered immunity (PTI), mediated by pattern recognition receptors (PRRs) and effector‐triggered immunity (ETI), mediated by the specific disease resistance (R) proteins that recognize avirulence (AVR) effectors (Chisholm et al , ; Jones and Dangl, ; Dodds and Rathjen, ; Boutrot and Zipfel, ; Cesari, ; Han, ). In plants, perception of PAMPs or effectors activates a complicated signal transduction network, including mitogen‐activated protein kinase (MAPK) cascades, and/or chemical signalling by plant hormones and transcriptional regulation via transcription factors (Pitzschke et al , ; Wang et al ., ).…”

Section: Introductionmentioning

confidence: 99%

An RXLR effector PlAvh142 from Peronophythora litchii triggers plant cell death and contributes to virulence

Situ

Jiang

Fan

et al. 2020

Molecular Plant Pathology

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Litchi downy blight, caused by the phytopathogenic oomycete Peronophythora litchii, results in tremendous economic loss in litchi production every year. To successfully colonize the host cell, Phytophthora species secret hundreds of RXLR effectors that interfere with plant immunity and facilitate the infection process. Previous work has already predicted 245 candidate RXLR effector‐encoding genes in P. litchii, 212 of which have been cloned and tested for plant cell death‐inducing activity in this study. We found three such RXLR effectors could trigger plant cell death through transient expression in Nicotiana benthamiana. Further experiments demonstrated that PlAvh142 could induce cell death and immune responses in several plants. We also found that PlAvh142 localized in both the cytoplasm and nucleus of plant cells. The cytoplasmic localization was critical for its cell death‐inducing activity. Moreover, deletion either of the two internal repeats in PlAvh142 abolished the cell death‐inducing activity. Virus‐induced gene silencing assays showed that cell death triggered by PlAvh142 was dependent on the plant transduction components RAR1 (require for Mla12 resistance), SGT1 (suppressor of the G2 allele of skp1) and HSP90 (heat shock protein 90). Finally, knockout of PlAvh142 resulted in significantly attenuated P. litchii virulence on litchi plants, whereas the PlAvh142‐overexpressed mutants were more aggressive. These data indicated that PlAvh142 could be recognized in plant cytoplasm and is an important virulence RXLR effector of P. litchii.

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Section: Introductionmentioning

confidence: 99%

An RXLR effector PlAvh142 from Peronophythora litchii triggers plant cell death and contributes to virulence

Situ

Jiang

Fan

et al. 2020

Molecular Plant Pathology

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“…At the center of the co-evolutionary dynamics between pathogens and plants are effector proteins, i.e. secreted proteins that manipulate host processes to facilitate infection and colonization [32][33][34][35].In return, host plants have evolved immune receptors that can detect conserved molecular patterns and effector proteins to defend against invading pathogens [36,37]. This generally leads to fast-paced co-evolution between pathogens and their host plants that often follows arms-race dynamics where the frequency of adaptive mutations rises quickly in pathogen populations [16].…”

Section: Introductionmentioning

confidence: 99%

Genomic rearrangements generate hypervariable mini-chromosomes in host-specific lineages of the blast fungus

Langner

Harant

Gómez-Luciano

et al. 2020

Preprint

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Supernumerary mini-chromosomes-a unique type of genomic structural variation-have been implicated in the emergence of virulence traits in plant pathogenic fungi. However, the mechanisms that facilitate the emergence and maintenance of mini-chromosomes across fungi remain poorly understood. In the blast fungus Magnaporthe oryzae, mini-chromosomes have been first described in the early 1990s but, until very recently, have been overlooked in genomic studies. Here we investigated structural variation in four isolates of the blast fungus M. oryzae from different grass hosts and analyzed the sequences of mini-chromosomes in the rice, foxtail millet and goosegrass isolates. The mini-chromosomes of these isolates turned out to be highly diverse with distinct sequence composition. They are enriched in repetitive elements and have lower gene density than core-chromosomes. We identified several virulence-related genes in the mini-chromosome of the rice isolate, including the polyketide synthase Ace1 and the effector gene AVR-Pik. Macrosynteny analyses around these loci revealed structural rearrangements, including inter-chromosomal translocations between core-and mini-chromosomes. Our findings provide evidence that mini-chromosomes independently emerge from structural rearrangements of core-chromosomes and might contribute to adaptive evolution of the blast fungus. Author summaryThe genomes of plant pathogens often exhibit an architecture that facilitates high rates of dynamic rearrangements and genetic diversification in virulence associated regions. These regions, which tend to be gene sparse and repeat rich, are thought to serve as a cradle for adaptive evolution. Supernumerary chromosomes, i.e. chromosomes that are only present in some but not all individuals of a species, are a special type of structural variation that have been observed in plants, animals, and fungi. Here we identified and studied supernumerary mini-chromosomes in the blast fungus Magnaporthe oryzae, a pathogen that causes some of the most destructive plant diseases. We found that rice, foxtail millet and goosegrass isolates of this pathogen contain mini-chromosomes with distinct sequence composition. All minichromosomes are rich in repetitive genetic elements and have lower gene densities than core-chromosomes. Further, we identified virulence-related genes on the mini-chromosome of the rice isolate. We observed large-scale genomic rearrangements around these loci, indicative of a role of mini-chromosomes in facilitating genome dynamics. Taken together, our results indicate that mini-chromosomes facilitate genome rearrangements and possibly adaptive evolution of the blast fungus.

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“…Where known, at least one of the causal loci encodes an immune protein, often an intracellular nucleotide binding site-leucine-rich repeat (NLR) protein [14][15][16][17][18][19][20][21][22][23]. The gene family encoding NLR immune receptors is the most variable gene family in plants, both in terms of inter-and intraspecific variation [24][25][26][27]. Many NLR proteins function as major disease resistance (R) proteins, with the extravagant variation at these loci being due to a combination of maintenance of very old alleles by long-term balancing selection and rapid evolution driven by strong diversifying selection [28][29][30].…”

Section: Introductionmentioning

confidence: 99%

RPW8/HR Repeats Predict NLR-dependent Hybrid Performance

Barragan

et al. 2019

Preprint

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Keywords RPW8, NLR, natural variation, autoimmunity, hybrid performance, MLKL, HET-S Barragan et al. RPW8/HR repeats and hybrid necrosis 2 SummaryHybrid offspring can look very different from their parents, including having greatly increased or decreased fitness. In many plant species, conflicts between divergent elements of the immune system can cause hybrids to express autoimmunity, a generally deleterious syndrome known as hybrid necrosis. We are investigating multiple hybrid necrosis cases in Arabidopsis thaliana that are caused by allele-specific interactions between different variants at two unlinked resistance (R) gene clusters. One is the RESISTANCE TO PERONOSPORA PARASITICA 7 (RPP7) cluster, which encodes an intracellular nucleotide binding site-leucine rich repeat (NLR) immune receptors that confer strain-specific resistance to oomycetes. The other is the RESISTANCE TO POWDERY MILDEW 8 (RPW8)/HOMOLOG OF RPW8 (HR) locus, which encodes atypical resistance proteins that can confer broad-spectrum resistance to filamentous pathogens. There is extensive structural variation in the RPW8/HR cluster, both at the level of gene copy number and at the level of C-terminal protein repeats of unknown function. We demonstrate that the number of RPW8/HR repeats correlate, albeit in a complex manner, with the severity of hybrid necrosis when these alleles are combined with specific RPP7 variants. This observation suggests that gross structural differences, rather than individual amino acid polymorphisms, guide the genetic interaction between RPW8/HR and RPP7 alleles. We discuss these findings in light of the similarity of RPW8/HR proteins with pore-forming toxins, MLKL and HET-S, from mammals and fungi.

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Multiple strategies for pathogen perception by plant immune receptors

Cited by 214 publications

References 43 publications

An RXLR effector PlAvh142 from Peronophythora litchii triggers plant cell death and contributes to virulence

An RXLR effector PlAvh142 from Peronophythora litchii triggers plant cell death and contributes to virulence

Genomic rearrangements generate hypervariable mini-chromosomes in host-specific lineages of the blast fungus

RPW8/HR Repeats Predict NLR-dependent Hybrid Performance

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