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The effector AvrRxo1 phosphorylates NAD in planta
- Source :
- PLoS Pathogens, Vol 13, Iss 6, p e1006442 (2017), PLoS Pathogens
- Publication Year :
- 2017
- Publisher :
- Public Library of Science (PLoS), 2017.
-
Abstract
- Gram-negative bacterial pathogens of plants and animals employ type III secreted effectors to suppress innate immunity. Most characterized effectors work through modification of host proteins or transcriptional regulators, although a few are known to modify small molecule targets. The Xanthomonas type III secreted avirulence factor AvrRxo1 is a structural homolog of the zeta toxin family of sugar-nucleotide kinases that suppresses bacterial growth. AvrRxo1 was recently reported to phosphorylate the central metabolite and signaling molecule NAD in vitro, suggesting that the effector might enhance bacterial virulence on plants through manipulation of primary metabolic pathways. In this study, we determine that AvrRxo1 phosphorylates NAD in planta, and that its kinase catalytic sites are necessary for its toxic and resistance-triggering phenotypes. A global metabolomics approach was used to independently identify 3’-NADP as the sole detectable product of AvrRxo1 expression in yeast and bacteria, and NAD kinase activity was confirmed in vitro. 3’-NADP accumulated upon transient expression of AvrRxo1 in Nicotiana benthamiana and in rice leaves infected with avrRxo1-expressing strains of X. oryzae. Mutation of the catalytic aspartic acid residue D193 abolished AvrRxo1 kinase activity and several phenotypes of AvrRxo1, including toxicity in yeast, bacteria, and plants, suppression of the flg22-triggered ROS burst, and ability to trigger an R gene-mediated hypersensitive response. A mutation in the Walker A ATP-binding motif abolished the toxicity of AvrRxo1, but did not abolish the 3’-NADP production, virulence enhancement, ROS suppression, or HR-triggering phenotypes of AvrRxo1. These results demonstrate that a type III effector targets the central metabolite and redox carrier NAD in planta, and that this catalytic activity is required for toxicity and suppression of the ROS burst.<br />Author summary Infectious bacteria have many strategies to weaken the defenses of their hosts. One common strategy is to inject proteins called effectors into the host cells. Many effectors inactivate proteins that transmit defense signals, disabling the alarm systems that alert the plant to defend against the pathogen. In this paper, we show that pathogens can also target very important small molecules in eukaryotes. We found that the plant pathogen effector AvrRxo1 adds a modification to NAD, a molecule required for hundreds of respiratory and signaling reactions, when expressed inside yeast or plant cells. This modification produces an unusual molecule, 3’-NADP, that is not able to be used efficiently by the cell. This finding demonstrates a new way that effectors can target essential central metabolites to manipulate the host.
- Subjects :
- 0301 basic medicine
Leaves
Nicotiana benthamiana
Yeast and Fungal Models
Plant Science
Toxicology
Pathology and Laboratory Medicine
Biochemistry
Metabolites
Medicine and Health Sciences
Phosphorylation
lcsh:QH301-705.5
Virulence
biology
Plant Bacterial Pathogens
Effector
Kinase
Plant Anatomy
Fungal Diseases
Plants
Infectious Diseases
Experimental Organism Systems
Saccharomyces Cerevisiae
Research Article
Hypersensitive response
lcsh:Immunologic diseases. Allergy
Xanthomonas
Immunology
Plant Pathogens
Research and Analysis Methods
Immune Suppression
Microbiology
Saccharomyces
03 medical and health sciences
Model Organisms
Signs and Symptoms
Bacterial Proteins
Plant and Algal Models
Diagnostic Medicine
Virology
Tobacco
Genetics
Grasses
Kinase activity
Molecular Biology
Plant Diseases
NAD+ kinase activity
Toxicity
Phosphotransferases
Organisms
Fungi
Biology and Life Sciences
Oryza
Plant Pathology
NAD
biology.organism_classification
Yeast
Metabolism
Yeast Infections
030104 developmental biology
lcsh:Biology (General)
Parasitology
Rice
NAD+ kinase
lcsh:RC581-607
Subjects
Details
- Language :
- English
- ISSN :
- 15537374 and 15537366
- Volume :
- 13
- Issue :
- 6
- Database :
- OpenAIRE
- Journal :
- PLoS Pathogens
- Accession number :
- edsair.doi.dedup.....01629b7b2fe970f3f069a5ba995f22c2