Plants are continuously threatened by pathogen attack and, as such, they have evolved mechanisms to evade, escape and defend themselves against pathogens. However, it is not known what types of ...defense mechanisms a plant would already possess to defend against a potential pathogen that has not co-evolved with the plant. We addressed this important question in a comprehensive manner by studying the responses of 1041 accessions of Arabidopsis thaliana to the foliar pathogen Pseudomonas syringae pv. tomato (Pst) DC3000.
We characterized the interaction using a variety of established methods, including different inoculation techniques, bacterial mutant strains, and assays for the hypersensitive response, salicylic acid (SA) accumulation and reactive oxygen species production.
Fourteen accessions showed resistance to infection by Pst DC3000. Of these, two accessions had a surface-based mechanism of resistance, six showed a hypersensitive-like response while three had elevated SA levels. Interestingly, A. thaliana was discovered to have a recognition system for the effector AvrPto, and HopAM1 was found to modulate Pst DC3000 resistance in two accessions.
Our comprehensive study has significant implications for the understanding of natural disease resistance mechanisms at the species level and for the ecology and evolution of plant–pathogen interactions.
Bacterial pathogens can cause multiple plant diseases and plants rely on their innate immune system to recognize and actively respond to these microbes. The plant innate immune system comprises ...extracellular pattern recognition receptors that recognize conserved microbial patterns and intracellular nucleotide binding leucine-rich repeat (NLR) proteins that recognize specific bacterial effectors delivered into host cells. Plants lack the adaptive immune branch present in animals, but still afford flexibility to pathogen attack through systemic and transgenerational resistance. Here, we focus on current research in plant immune responses against bacterial pathogens. Recent studies shed light onto the activation and inactivation of pattern recognition receptors and systemic acquired resistance. New research has also uncovered additional layers of complexity surrounding NLR immune receptor activation, cooperation and sub-cellular localizations. Taken together, these recent advances bring us closer to understanding the web of molecular interactions responsible for coordinating defense responses and ultimately resistance.
Summary
The intracellular nucleotide‐binding domain leucine‐rich repeat (NLR) class of immune receptors plays an important role in plant viral defence. Plant NLRs recognize viruses through direct or ...indirect association of viral proteins, triggering a downstream defence response to prevent viral proliferation and movement within the plant. This review focuses on current knowledge of intracellular perception of viral pathogens, activation of NLRs and the downstream signalling components involved in plant viral defence.
Arabidopsis BAK1/SERK3, a co-receptor of leucine-rich repeat pattern recognition receptors (PRRs), mediates pattern-triggered immunity (PTI). Genetic inactivation of BAK1 or BAK1-interacting ...receptor-like kinases (BIRs) causes cell death, but the direct mechanisms leading to such deregulation remains unclear. Here, we found that the TIR-NBS-LRR protein CONSTITUTIVE SHADE AVOIDANCE 1 (CSA1) physically interacts with BIR3, but not with BAK1. CSA1 mediates cell death in bak1-4 and bak1-4 bir3-2 mutants via components of effector-triggered immunity-(ETI) pathways. Effector HopB1-mediated perturbation of BAK1 also results in CSA1-dependent cell death. Likewise, microbial pattern pg23-induced cell death, but not PTI responses, requires CSA1. Thus, we show that CSA1 guards BIR3 BAK1 homeostasis and integrates pattern- and effector-mediated cell death pathways downstream of BAK1. De-repression of CSA1 in the absence of intact BAK1 and BIR3 triggers ETI cell death. This suggests that PTI and ETI pathways are activated downstream of BAK1 for efficient plant immunity.
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•BAK1 and BIR3 perturbation is guarded by the TNL CSA1•BAK1 surveillance by CSA1 is required for PRR- and an NLR-receptor-initiated cell death•CSA1 contributes to PTI, but classical PTI responses are not altered in csa1 mutants•Both ETI- and PTI-type defense pathways are activated downstream of BAK1
Schulze, Yu, et al. show that CSA1 mediates cell death initiated by BAK1 inactivation. This cell death is triggered by pattern recognition by cell surface receptors and an effector, recognized by CSA1. Both initiate BAK1 cleavage, indicating that surveillance of BAK1 leads to activation of ETI-type cell death via CSA1.
Plants face a relentless onslaught from a diverse array of pathogens in their natural environment, to which they have evolved a myriad of strategies that unfold across various temporal scales. Cell ...surface pattern recognition receptors (PRRs) detect conserved elicitors from pathogens or endogenous molecules released during pathogen invasion, initiating the first line of defence in plants, known as pattern-triggered immunity (PTI), which imparts a baseline level of disease resistance. Inside host cells, pathogen effectors are sensed by the nucleotide-binding/leucine-rich repeat (NLR) receptors, which then activate the second line of defence: effector-triggered immunity (ETI), offering a more potent and enduring defence mechanism. Moreover, PTI and ETI collaborate synergistically to bolster disease resistance and collectively trigger a cascade of downstream defence responses. This article provides a comprehensive review of plant defence responses, offering an overview of the stepwise activation of plant immunity and the interactions between PTI-ETI synergistic signal transduction.
•Biomolecules from plant innate immunity can be used to engineer disease-resistant plants.•Biomolecules include plant immunity/defense proteins in addition to pathogen effectors.•The pros and cons of ...these biomolecules for transgenic approaches are discussed.
This review emphasizes the biotechnological potential of molecules implicated in the different layers of plant immunity, including, pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI), effector-triggered susceptibility (ETS), and effector-triggered immunity (ETI) that can be applied in the development of disease-resistant genetically modified (GM) plants. These biomolecules are produced by pathogens (viruses, bacteria, fungi, oomycetes) or plants during their mutual interactions. Biomolecules involved in the first layers of plant immunity, PTI and ETS, include inhibitors of pathogen cell-wall-degrading enzymes (CWDEs), plant pattern recognition receptors (PRRs) and susceptibility (S) proteins, while the ETI-related biomolecules include plant resistance (R) proteins. The biomolecules involved in plant defense PTI/ETI responses described herein also include antimicrobial peptides (AMPs), pathogenesis-related (PR) proteins and ribosome-inhibiting proteins (RIPs), as well as enzymes involved in plant defensive secondary metabolite biosynthesis (phytoanticipins and phytoalexins). Moreover, the regulation of immunity by RNA interference (RNAi) in GM disease-resistant plants is also considered. Therefore, the present review does not cover all the classes of biomolecules involved in plant innate immunity that may be applied in the development of disease-resistant GM crops but instead highlights the most common strategies in the literature, as well as their advantages and disadvantages.
In natural habitats, plants are exploited by pathogens in biotrophic or necrotrophic ways. Concurrently, plants have evolved their defense systems for rapid perception of pathogenic effectors and ...begin concerted cellular reprogramming pathways to confine the pathogens at the entry sites. During the reorganization of cellular signaling mechanisms following pathogen attack, non-coding RNAs serves an indispensable role either as a source of resistance or susceptibility. Besides the well-studied functions of non-coding RNAs related to plant development and abiotic stress responses, previous and recent discoveries have established that non-coding RNAs like miRNAs, siRNAs, lncRNAs and phasi-RNAs can fine tune plant defense responses by targeting various signaling pathways. In this review, recapitulation of previous reports associated with non-coding RNAs as a defense responder against virus, bacteria and fungus attacks and insightful discussion will lead us to conceive innovative ideas to fight against approaching threats of resistant breaking pathogens.
•Non-coding RNAs play vital role in providing susceptibility/tolerance to plant pathogens.•They target components of defense pathways such as phytohormone and ROS signaling pathways.•They modulate gene expression during plant-pathogen interaction.•They maintain the trade-off between plant growth and defense.
Resistance against oomycete pathogens is mainly governed by intracellular nucleotide-binding leucine-rich repeat (NLR) receptors that recognize matching avirulence (AVR) proteins from the pathogen, ...RXLR effectors that are delivered inside host cells. Detailed molecular understanding of how and where NLR proteins and RXLR effectors interact is essential to inform the deployment of durable resistance (R) genes.
Fluorescent tags, nuclear localization signals (NLSs) and nuclear export signals (NESs) were exploited to determine the subcellular localization of the potato late blight protein R1 and the Phytophthora infestans RXLR effector AVR1, and to target these proteins to the nucleus or cytoplasm.
Microscopic imaging revealed that both R1 and AVR1 occurred in the nucleus and cytoplasm, and were in close proximity. Transient expression of NLS- or NES-tagged R1 and AVR1 in Nicotiana benthamiana showed that activation of the R1-mediated hypersensitive response and resistance required localization of the R1/AVR1 pair in the nucleus. However, AVR1-mediated suppression of cell death in the absence of R1 was dependent on localization of AVR1 in the cytoplasm. Balanced nucleocytoplasmic partitioning of AVR1 seems to be a prerequisite.
Our results show that R1-mediated immunity is activated inside the nucleus with AVR1 in close proximity and suggest that nucleocytoplasmic transport of R1 and AVR1 is tightly regulated.
•ETI affects de-novo synthesis of sphingolipids by altering the ceramides/dihydroceramides ratio•This effect is independent of the genotype and independent of CFTR rescue and functions•The effect is ...consistent with the inhibition of ceramide desaturase enzymes•Potential long-term safety concerns due to dihydrosphingolipid accumulation should be assessed
We report here how the triple combination of drugs elexacaftor/tezacaftor/ivacaftor (ETI) alters the balance of the de-novo synthethic pathway of sphingolipids in primary cells of human bronchial epithelium. The treatment with ETI roughly doubles the levels of dihydrosphingolipids, possibly by modulating the delta(4)-desaturase enzymes that convert dihydroceramides into ceramides. This appears to be an off-target effect of ETI, since it occurs in a genotype-independent manner, for both cystic fibrosis (CF) and non-CF subjects.
SUMMARY
Arabidopsis pathogen effector‐triggered immunity (ETI) is controlled by a family of three lipase‐like proteins (EDS1, PAD4, and SAG101) and two subfamilies of HET‐S/LOB‐B (HeLo)‐domain ...“helper” nucleotide‐binding/leucine‐rich repeats (ADR1s and NRG1s). EDS1‐PAD4 dimers cooperate with ADR1s, and EDS1‐SAG101 dimers with NRG1s, in two separate defense‐promoting modules. EDS1‐PAD4‐ADR1 and EDS1‐SAG101‐NRG1 complexes were detected in immune‐activated leaf extracts but the molecular determinants for specific complex formation and function remain unknown. EDS1 signaling is mediated by a C‐terminal EP domain (EPD) surface surrounding a cavity formed by the heterodimer. Here we investigated whether the EPDs of PAD4 and SAG101 contribute to EDS1 dimer functions. Using a structure‐guided approach, we undertook a comprehensive mutational analysis of Arabidopsis PAD4. We identify two conserved residues (Arg314 and Lys380) lining the PAD4 EPD cavity that are essential for EDS1‐PAD4–mediated pathogen resistance, but are dispensable for the PAD4‐mediated restriction of green peach aphid infestation. Positionally equivalent Met304 and Arg373 at the SAG101 EPD cavity are required for EDS1‐SAG101 promotion of ETI‐related cell death. In a PAD4 and SAG101 interactome analysis of ETI‐activated tissues, PAD4R314A and SAG101M304R EPD variants maintain interaction with EDS1 but lose association, respectively, with helper nucleotide‐binding/leucine‐rich repeats ADR1‐L1 and NRG1.1, and other immune‐related proteins. Our data reveal a fundamental contribution of similar but non‐identical PAD4 and SAG101 EPD surfaces to specific EDS1 dimer protein interactions and pathogen immunity.
Significance Statement
The molecular determinants for EDS1‐PAD4‐ADR1 and EDS1‐SAG101‐NRG1 complex formation and function remain unknown. In a PAD4 and SAG101 interactome analysis of ETI‐activated tissues, PAD4R314A and SAG101M304R EPD variants maintain interaction with EDS1 but lose association, respectively, with helper NLRs ADR1‐L1 and NRG1.1, and other immune‐related proteins, this reveals a fundamental contribution of similar but non‐identical PAD4 and SAG101 EPD surfaces to specific EDS1 dimer protein interactions and pathogen immunity.
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