Study on the regulation of broad‐spectrum resistance is an active area in plant biology.
- Award ID(s):
- 1901566
- NSF-PAR ID:
- 10388426
- Date Published:
- Journal Name:
- New Phytologist
- ISSN:
- 0028-646X
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
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Abstract RESISTANCE TO POWDERY MILDEW 8.1 (RPW8.1 ) is one of a few broad‐spectrum resistance genes triggering the hypersensitive response (HR) to restrict multiple pathogenic infections. To address the question how RPW8.1 signaling is regulated, we performed a genetic screen and tried to identify mutations enhancing RPW8.1‐mediated HR. Here, we provided evidence to connect an annexin protein with RPW8.1‐mediated resistance inArabidopsis against powdery mildew. We isolated and characterizedArabidopsis b7‐6 mutant. A point mutation inb7‐6 at theAt5g12380 locus resulted in an amino acid substitution in ANNEXIN 8 (AtANN8). Loss‐of‐function or RNA‐silencing ofAtANN8 led to enhanced expression ofRPW8.1 , RPW8.1‐dependent necrotic lesions in leaves, and defense against powdery mildew. Conversely, over‐expression ofAtANN8 compromised RPW8.1‐mediated disease resistance and cell death. Interestingly, the mutation in AtANN8 enhanced RPW8.1‐triggered H2O2. In addition, mutation in AtANN8 led to hypersensitivity to salt stress. Together, our data indicate that AtANN8 is involved in multiple stress signaling pathways and negatively regulates RPW8.1‐mediated resistance against powdery mildew and cell death, thus linking ANNEXIN's function with plant immunity. -
Abstract The actin‐related protein 2/3 complex (Arp2/3 complex), a key regulator of actin cytoskeletal dynamics, has been linked to multiple cellular processes, including those associated with response to stress. Herein, the
gene, encoding a subunit protein of the Arp2/3 complex, was identified and characterized.Solanum habrochaites ARPC3ShARPC3 encodes a 174‐amino acid protein possessing a conserved P21‐Arc domain. Silencing ofShARPC3 resulted in enhanced susceptibility to the powdery mildew pathogen (Oidium neolycopersici On ‐Lz), demonstrating a role forShARPC3 in defence signalling. Interestingly, a loss ofShARPC3 coincided with enhanced susceptibility toOn ‐Lz, a process that we hypothesize is the result of a block in the activity of SA‐mediated defence signalling. Conversely, overexpression ofShARPC3 in , followed by inoculation withArabidopsis thaliana On ‐Lz, showed enhanced resistance, including the rapid induction of hypersensitive cell death and the generation of reactive oxygen. Heterologous expression ofShARPC3 in thearc18 mutant of (i.e.,Saccharomyces cerevisiae ∆arc18 ) resulted in complementation of stress‐induced phenotypes, including high‐temperature tolerance. Taken together, these data support a role for ShARPC3 in tomato through positive regulation of plant immunity in response toO .neolycopersici pathogenesis. -
Abstract Nonhost resistance (NHR) refers to the immunity of most tested genotypes of a plant species to most tested variants of a pathogen species. Thus, NHR is broad spectrum and durable in nature and constitutes a major safety barrier against invasion of a myriad of potentially pathogenic microbes in any plants including domesticated crops. Genetic study of NHR is generally more difficult compared to host resistance mainly because NHR is genetically more complicated and often lacks intraspecific polymorphisms. Nevertheless, substantial progress has been made towards the understanding of the molecular basis of NHR in the past two decades using various approaches. Not surprisingly, molecular mechanisms of NHR revealed so far encompasses pathogen‐associated molecular pattern‐triggered immunity and effector‐triggered immunity. In this review, we briefly discuss the inherent difficulty in genetic studies of NHR and summarize the main approaches that have been taken to identify genes contributing to NHR. We also discuss new enabling strategies for dissecting multilayered NHR in model plants with a focus on NHR against filamentous pathogens, especially biotrophic pathogens such as powdery mildew and rust fungi.
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Abstract Plant pathogens use effector proteins to target host processes involved in pathogen perception, immune signalling, or defence outputs. Unlike foliar pathogens, it is poorly understood how root‐invading pathogens suppress immunity. The Avr2 effector from the tomato root‐ and xylem‐colonizing pathogen
Fusarium oxysporum suppresses immune signalling induced by various pathogen‐associated molecular patterns (PAMPs). It is unknown how Avr2 targets the immune system. TransgenicAVR2 Arabidopsis thaliana phenocopies mutants in which the pattern recognition receptor (PRR) co‐receptor BRI1‐ASSOCIATED RECEPTOR KINASE (BAK1) or its downstream signalling kinase BOTRYTIS‐INDUCED KINASE 1 (BIK1) are knocked out. We therefore tested whether these kinases are Avr2 targets. Flg22‐induced complex formation of the PRR FLAGELLIN SENSITIVE 2 and BAK1 occurred in the presence and absence of Avr2, indicating that Avr2 does not affect BAK1 function or PRR complex formation. Bimolecular fluorescence complementation assays showed that Avr2 and BIK1 co‐localize in planta. Although Avr2 did not affect flg22‐induced BIK1 phosphorylation, mono‐ubiquitination was compromised. Furthermore, Avr2 affected BIK1 abundance and shifted its localization from nucleocytoplasmic to the cell periphery/plasma membrane. Together, these data imply that Avr2 may retain BIK1 at the plasma membrane, thereby suppressing its ability to activate immune signalling. Because mono‐ubiquitination of BIK1 is required for its internalization, interference with this process by Avr2 could provide a mechanistic explanation for the compromised BIK1 mobility upon flg22 treatment. The identification of BIK1 as an effector target of a root‐invading vascular pathogen identifies this kinase as a conserved signalling component for both root and shoot immunity. -
Summary Biotrophic pathogens are believed to strategically manipulate sugar transport in host cells to enhance their access to carbohydrates. However, mechanisms of sugar translocation from host cells to biotrophic fungi such as powdery mildew across the plant–haustorium interface remain poorly understood.
To investigate this question, systematic subcellular localisation analysis was performed for all the 14 members of the monosaccharide sugar transporter protein (STP) family in
Arabidopsis thaliana . The best candidate AtSTP8 was further characterised for its transport properties inSaccharomyces cerevisiae and potential role in powdery mildew infection by gene ablation and overexpression in Arabidopsis.Our results showed that AtSTP8 was mainly localised to the endoplasmic reticulum (ER) and appeared to be recruited to the host‐derived extrahaustorial membrane (EHM) induced by powdery mildew. Functional complementation assays in
S. cerevisiae suggested that AtSTP8 can transport a broad spectrum of hexose substrates. Moreover, transgenic Arabidopsis plants overexpressingAtSTP8 showed increased hexose concentration in leaf tissues and enhanced susceptibility to powdery mildew.Our data suggested that the ER‐localised sugar transporter AtSTP8 may be recruited to the EHM where it may be involved in sugar acquisition by haustoria of powdery mildew from host cells in Arabidopsis.