Author
Ryan G. Anderson
Other affiliations: United States Department of Agriculture, University of North Carolina at Chapel Hill, Natural Resources Canada ...read more
Bio: Ryan G. Anderson is an academic researcher from Virginia Tech. The author has contributed to research in topics: Effector & Hyaloperonospora arabidopsidis. The author has an hindex of 13, co-authored 21 publications receiving 1583 citations. Previous affiliations of Ryan G. Anderson include United States Department of Agriculture & University of North Carolina at Chapel Hill.
Papers
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University of Warwick1, Virginia Bioinformatics Institute2, University of East Anglia3, Utrecht University4, Goethe University Frankfurt5, John Innes Centre6, University of California, Riverside7, Virginia Tech8, University of California, Berkeley9, Lawrence Berkeley National Laboratory10, Washington University in St. Louis11, Nanjing Agricultural University12, Agriculture and Agri-Food Canada13, University of Toulouse14, Centre national de la recherche scientifique15, Wageningen University and Research Centre16, Wellcome Trust17, Broad Institute18, Bowling Green State University19
TL;DR: The genome sequence of the oomycete Hyaloperonospora arabidopsidis is reported, an obligate biotroph and natural pathogen of Arabidopsis thaliana, which exhibits dramatic reductions in genes encoding RXLR effectors, proteins associated with zoospore formation and motility, and enzymes for assimilation of inorganic nitrogen and sulfur.
Abstract: Many oomycete and fungal plant pathogens are obligate biotrophs, which extract nutrients only from living plant tissue and cannot grow apart from their hosts. Although these pathogens cause substantial crop losses, little is known about the molecular basis or evolution of obligate biotrophy. Here, we report the genome sequence of the oomycete Hyaloperonospora arabidopsidis (Hpa), an obligate biotroph and natural pathogen of Arabidopsis thaliana. In comparison with genomes of related, hemibiotrophic Phytophthora species, the Hpa genome exhibits dramatic reductions in genes encoding (i) RXLR effectors and other secreted pathogenicity proteins, (ii) enzymes for assimilation of inorganic nitrogen and sulfur, and (iii) proteins associated with zoospore formation and motility. These attributes comprise a genomic signature of evolution toward obligate biotrophy.
424 citations
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TL;DR: It is demonstrated that plant Toll/interleukin-1 receptor (TIR) domains of NLRs are enzymes capable of degrading nicotinamide adenine dinucleotide in its oxidized form (NAD+); both cell death induction and NAD+ cleavage activity of plant TIR domains require known self-association interfaces.
Abstract: Plant nucleotide-binding leucine-rich repeat (NLR) immune receptors activate cell death and confer disease resistance by unknown mechanisms. We demonstrate that plant Toll/interleukin-1 receptor (TIR) domains of NLRs are enzymes capable of degrading nicotinamide adenine dinucleotide in its oxidized form (NAD+). Both cell death induction and NAD+ cleavage activity of plant TIR domains require known self-association interfaces and a putative catalytic glutamic acid that is conserved in both bacterial TIR NAD+-cleaving enzymes (NADases) and the mammalian SARM1 (sterile alpha and TIR motif containing 1) NADase. We identify a variant of cyclic adenosine diphosphate ribose as a biomarker of TIR enzymatic activity. TIR enzymatic activity is induced by pathogen recognition and functions upstream of the genes enhanced disease susceptibility 1 (EDS1) and N requirement gene 1 (NRG1), which encode regulators required for TIR immune function. Thus, plant TIR-NLR receptors require NADase function to transduce recognition of pathogens into a cell death response.
304 citations
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TL;DR: This work shows that the Phytophthora sojae effector protein Avr1b can contribute positively to virulence and can suppress programmed cell death triggered by the mouse BAX protein in yeast, soybean, and Nicotiana benthamiana cells, and supports the hypothesis that these motifs are critical for the functions of the very large number of predicted oomycete effectors that contain them.
Abstract: The sequenced genomes of oomycete plant pathogens contain large superfamilies of effector proteins containing the protein translocation motif RXLR-dEER. However, the contributions of these effectors to pathogenicity remain poorly understood. Here, we show that the Phytophthora sojae effector protein Avr1b can contribute positively to virulence and can suppress programmed cell death (PCD) triggered by the mouse BAX protein in yeast, soybean (Glycine max), and Nicotiana benthamiana cells. We identify three conserved motifs (K, W, and Y) in the C terminus of the Avr1b protein and show that mutations in the conserved residues of the W and Y motifs reduce or abolish the ability of Avr1b to suppress PCD and also abolish the avirulence interaction of Avr1b with the Rps1b resistance gene in soybean. W and Y motifs are present in at least half of the identified oomycete RXLR-dEER effector candidates, and we show that three of these candidates also suppress PCD in soybean. Together, these results indicate that the W and Y motifs are critical for the interaction of Avr1b with host plant target proteins and support the hypothesis that these motifs are critical for the functions of the very large number of predicted oomycete effectors that contain them.
300 citations
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TL;DR: It is shown that Exo70B2 is required for both immediate and later responses triggered by all tested PAMPs, suggestive of a role in signaling, and proposed mechanism by which PUB22-mediated degradation of Exo 70B2 contributes to the attenuation of PAMP-induced signaling.
Abstract: Plant pathogens are perceived by pattern recognition receptors, which are activated upon binding to pathogen-associated molecular patterns (PAMPs). Ubiquitination and vesicle trafficking have been linked to the regulation of immune signaling. However, little information exists about components of vesicle trafficking involved in immune signaling and the mechanisms that regulate them. In this study, we identified Arabidopsis thaliana Exo70B2, a subunit of the exocyst complex that mediates vesicle tethering during exocytosis, as a target of the plant U-box–type ubiquitin ligase 22 (PUB22), which acts in concert with PUB23 and PUB24 as a negative regulator of PAMP-triggered responses. We show that Exo70B2 is required for both immediate and later responses triggered by all tested PAMPs, suggestive of a role in signaling. Exo70B2 is also necessary for the immune response against different pathogens. Our data demonstrate that PUB22 mediates the ubiquitination and degradation of Exo70B2 via the 26S Proteasome. Furthermore, degradation is regulated by the autocatalytic turnover of PUB22, which is stabilized upon PAMP perception. We therefore propose a mechanism by which PUB22-mediated degradation of Exo70B2 contributes to the attenuation of PAMP-induced signaling.
190 citations
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TL;DR: It is shown that the defense role of CCA1 and LHY against P. syringae is at least partially through circadian control of stomatal aperture but is independent of defense mediated by salicylic acid, and crosstalk between the circadian clock and plant innate immunity is revealed for the first time.
Abstract: The circadian clock integrates temporal information with environmental cues in regulating plant development and physiology Recently, the circadian clock has been shown to affect plant responses to biotic cues To further examine this role of the circadian clock, we tested disease resistance in mutants disrupted in CCA1 and LHY, which act synergistically to regulate clock activity We found that cca1 and lhy mutants also synergistically affect basal and resistance gene-mediated defense against Pseudomonas syringae and Hyaloperonospora arabidopsidis Disrupting the circadian clock caused by overexpression of CCA1 or LHY also resulted in severe susceptibility to P syringae We identified a downstream target of CCA1 and LHY, GRP7, a key constituent of a slave oscillator regulated by the circadian clock and previously shown to influence plant defense and stomatal activity We show that the defense role of CCA1 and LHY against P syringae is at least partially through circadian control of stomatal aperture but is independent of defense mediated by salicylic acid Furthermore, we found defense activation by P syringae infection and treatment with the elicitor flg22 can feedback-regulate clock activity Together this data strongly supports a direct role of the circadian clock in defense control and reveal for the first time crosstalk between the circadian clock and plant innate immunity
163 citations
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28 Jul 2005
TL;DR: PfPMP1)与感染红细胞、树突状组胞以及胎盘的单个或多个受体作用,在黏附及免疫逃避中起关键的作�ly.
Abstract: 抗原变异可使得多种致病微生物易于逃避宿主免疫应答。表达在感染红细胞表面的恶性疟原虫红细胞表面蛋白1(PfPMP1)与感染红细胞、内皮细胞、树突状细胞以及胎盘的单个或多个受体作用,在黏附及免疫逃避中起关键的作用。每个单倍体基因组var基因家族编码约60种成员,通过启动转录不同的var基因变异体为抗原变异提供了分子基础。
18,940 citations
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Broad Institute1, Ohio Agricultural Research and Development Center2, Sainsbury Laboratory3, Uppsala University4, Wageningen University and Research Centre5, Virginia Bioinformatics Institute6, University of California, Riverside7, University of Aberdeen8, Scottish Crop Research Institute9, University of Warwick10, Agricultural Research Service11, Royal Institute of Technology12, Cornell University13, Oregon State University14, Lafayette College15, University of Glasgow16, Harvard University17, Delaware Biotechnology Institute18, North Carolina State University19, University of Delaware20, University of Tennessee21, University of Maryland, Baltimore22, Vanderbilt University23, College of Wooster24, Bowling Green State University25, Edinburgh Cancer Research Centre26, J. Craig Venter Institute27, Tel Aviv University28, University of Wisconsin-Madison29, University of Hohenheim30, University of Dundee31
TL;DR: The sequence of the P. infestans genome is reported, which at ∼240 megabases (Mb) is by far the largest and most complex genome sequenced so far in the chromalveolates and probably plays a crucial part in the rapid adaptability of the pathogen to host plants and underpins its evolutionary potential.
Abstract: Phytophthora infestans is the most destructive pathogen of potato and a model organism for the oomycetes, a distinct lineage of fungus-like eukaryotes that are related to organisms such as brown algae and diatoms. As the agent of the Irish potato famine in the mid-nineteenth century, P. infestans has had a tremendous effect on human history, resulting in famine and population displacement(1). To this day, it affects world agriculture by causing the most destructive disease of potato, the fourth largest food crop and a critical alternative to the major cereal crops for feeding the world's population(1). Current annual worldwide potato crop losses due to late blight are conservatively estimated at $6.7 billion(2). Management of this devastating pathogen is challenged by its remarkable speed of adaptation to control strategies such as genetically resistant cultivars(3,4). Here we report the sequence of the P. infestans genome, which at similar to 240 megabases (Mb) is by far the largest and most complex genome sequenced so far in the chromalveolates. Its expansion results from a proliferation of repetitive DNA accounting for similar to 74% of the genome. Comparison with two other Phytophthora genomes showed rapid turnover and extensive expansion of specific families of secreted disease effector proteins, including many genes that are induced during infection or are predicted to have activities that alter host physiology. These fast-evolving effector genes are localized to highly dynamic and expanded regions of the P. infestans genome. This probably plays a crucial part in the rapid adaptability of the pathogen to host plants and underpins its evolutionary potential.
1,341 citations
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TL;DR: Recent developments point towards a multilayered plant innate immune system comprised of self-surveillance, systemic signalling and chromosomal changes that together establish effective immunity.
Abstract: Vertebrates have evolved a sophisticated adaptive immune system that relies on an almost infinite diversity of antigen receptors that are clonally expressed by specialized immune cells that roam the circulatory system. These immune cells provide vertebrates with extraordinary antigen-specific immune capacity and memory, while minimizing self-reactivity. Plants, however, lack specialized mobile immune cells. Instead, every plant cell is thought to be capable of launching an effective immune response. So how do plants achieve specific, self-tolerant immunity and establish immune memory? Recent developments point towards a multilayered plant innate immune system comprised of self-surveillance, systemic signalling and chromosomal changes that together establish effective immunity.
933 citations
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TL;DR: The mechanisms that fine-tune immune signalling to maintain immune homeostasis are described and how the innate ability of plant cells to monitor the integrity of key immune components can lead to autoimmune phenotypes following genetic or pathogen-induced perturbations of these components are discussed.
Abstract: Plants depend on cell-autonomous innate immune mechanisms for protection against infection and these pathways are activated in response to pattern recognition receptor (PRR) engagement. However, as is the case in mammals, PRR signalling in plants must be tightly controlled to avoid pathological outcomes; this Review focuses on the mechanisms that regulate plant PRR signalling.
841 citations
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TL;DR: An analysis of protein-protein interactions in Arabidopsis identifies the plant interactome and demonstrated plant immune system functions for 15 of 17 tested host proteins that interact with effectors from both pathogens.
Abstract: Plants generate effective responses to infection by recognizing both conserved and variable pathogen-encoded molecules. Pathogens deploy virulence effector proteins into host cells, where they interact physically with host proteins to modulate defense. We generated an interaction network of plant-pathogen effectors from two pathogens spanning the eukaryote-eubacteria divergence, three classes of Arabidopsis immune system proteins, and ~8000 other Arabidopsis proteins. We noted convergence of effectors onto highly interconnected host proteins and indirect, rather than direct, connections between effectors and plant immune receptors. We demonstrated plant immune system functions for 15 of 17 tested host proteins that interact with effectors from both pathogens. Thus, pathogens from different kingdoms deploy independently evolved virulence proteins that interact with a limited set of highly connected cellular hubs to facilitate their diverse life-cycle strategies.
739 citations