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Toll/interleukin-1/resistance (TIR) domain proteins contribute to innate immunity in all cellular kingdoms. TIR modules are activated by self-association and in plants, mammals and bacteria, some TIRs have enzymatic functions that are crucial for disease resistance and/or cell death. Many plant TIR-only proteins and pathogen effector-activated TIR-domain NLR receptors are NAD + hydrolysing enzymes. Biochemical, structural and functional studies established that for both plant TIR-protein types, and certain bacterial TIRs, NADase activity generates bioactive signalling intermediates which promote resistance. A set of plant TIR-catalysed nucleotide isomers was discovered which bind to and activate EDS1 complexes, promoting their interactions with co-functioning helper NLRs. Analysis of TIR enzymes across kingdoms fills an important gap in understanding how pathogen disturbance induces TIR-regulated immune responses., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Toll and interleukin-1 receptor (TIR) domain is a conserved immune module in prokaryotes and eukaryotes. Signaling regulated by TIR-only proteins or TIR domain-containing intracellular immune receptors is critical for plant immunity. Recent studies demonstrated that TIR domains function as enzymes encoding a variety of activities, which manifest different mechanisms for regulation of plant immunity. These enzymatic activities catalyze metabolism of NAD + , ATP and other nucleic acids, generating structurally diversified nucleotide metabolites. Signaling roles have been revealed for some TIR enzymatic products that can act as second messengers to induce plant immunity. Herein, we summarize our current knowledge about catalytic production of these nucleotide metabolites and their roles in plant immune signaling. We also highlight outstanding questions that are likely to be the focus of future investigations about TIR-produced signaling molecules., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

The conserved lipase-like protein EDS1 transduces signals from pathogen-activated intracellular nucleotide-binding leucine-rich repeat (NLR) receptors to transcriptional defences and host cell death. In this pivotal NLR signalling role, EDS1 works as a heterodimer with each of its partners, SAG101 and PAD4. Different properties of EDS1-SAG101 and EDS1-PAD4 complexes and functional relationships to sensor and helper NLRs have emerged. EDS1-SAG101 dimers confer effector-triggered immunity mediated by intracellular TNL receptors. In contrast, EDS1-PAD4 dimers have a broader role promoting basal immune responses that can be initiated inside cells by TNL- or CNL-type NLRs, and at the cell surface by LRR-receptor proteins. Characterizing the essential elements of these two EDS1 modules will help to connect intracellular and surface receptor signalling networks in the plant immune system., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2021 The Authors. Published by Elsevier Ltd.. All rights reserved.)

The plant immune system inhibits pathogen growth and contributes to shaping a healthy microbial community in the plant body. Plants must appropriately respond to both microbial signals and abiotic factors that are diverse in time and space, and thus, proper integration of these inputs at local and systemic levels is of crucial importance for optimal plant responses and fitness in nature. Here, we review our current knowledge of three properties of the plant immune system, resilience, tunability, and balance, which enable plants to deal with complex cocktails of environmental factors. We also discuss future challenges on the path towards a comprehensive understanding of the interactions between plant immunity and pathogenic, non-pathogenic, and beneficial microbes., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Rapid and massive transcriptional reprogramming upon pathogen recognition is the decisive step in plant-phytopathogen interactions. Plant transcription factors (TFs) are key players in this process but they require a suite of other context-specific co-regulators to establish sensory transcription regulatory networks to bring about host immunity. Molecular, genetic and biochemical studies, particularly in the model plants Arabidopsis and rice, are continuously uncovering new components of the transcriptional machinery that can selectively impact host resistance toward a diverse range of pathogens. Moreover, detailed studies on key immune regulators, such as WRKY TFs and NPR1, are beginning to reveal the underlying mechanisms by which defense hormones influence the function of these factors. Here we provide a short update on such recent developments., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Plant hormones regulate physiological responses in plants, including responses to pathogens and beneficial microbes. The last decades have provided a vast amount of evidence about the contribution of different plant hormones to plant immunity, and also of how they cooperate to orchestrate immunity activation, in a process known as hormone crosstalk. In this review we highlight the complexity of hormonal crosstalk in immunity and approaches currently being used to further understand this process, as well as perspectives to engineer hormone crosstalk for enhanced pathogen resistance and overall plant fitness., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

In plants, a large polymorphic family of intracellular NB-LRR receptors lies at the heart of robust resistance to diverse pathogens and mechanisms by which these versatile molecular switches operate in effector-triggered immunity are beginning to emerge. We outline recent advances in our understanding of NB-LRR receptor signaling leading to disease resistance. Themes covered are (i) NB-LRR molecular constraining forces and their intimate relationship with receptor activation in different parts of the cell, (ii) cooperativity between NB-LRR proteins and the formation of higher order NB-LRR signaling complexes, and (iii) the spatial separation of different resistance branches within cells. Finally, we examine evidence for dynamic signaling across cell compartments in coordinating diverse immune outputs., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

The sessile nature of flowering plants and their capacity to thrive in soil habitats likely resulted in specific adaptation mechanisms enabling co-existence with a vast diversity of air-borne and soil-borne microorganisms. Only a small fraction of these microbial encounters result in pathogenic or symbiotic interactions, whilst the majority appear to give rise to commensalistic or mutualistic associations. Considering the abundance of the latter associations the question arises whether plants evolved, besides the plant immune system, other dedicated mechanisms to communicate with and to host microbial communities in the phyllosphere and rhizosphere. We hypothesize that the constitutive and microbe-induced secretion of specialized plant-derived biomolecules creates a critical interface for all types of plant-microbe associations. Thus, the plant secretory machinery might serve an important role in establishing an extended phenotype with microbial life., (Copyright 2010 Elsevier Ltd. All rights reserved.)

Membrane specialization through lateral compartmentalization is pivotal to the development of organisms and their response to environmental signals. The membrane raft hypothesis is lively discussed as a concept for domain formation. In recent years plant scientists have begun to critically assess the membrane raft hypothesis, and this provided the first insights into the mechanisms underlying microdomain formation in plant plasma membranes. Several groups have now shown that phytosterols can induce phase separation, a prerequisite for the formation of membrane rafts. Furthermore, the protein repertoire of detergent-resistant membranes (DRMs) has been extensively characterized and the degree of fatty acid desaturation has been identified as an important factor in DRM formation. Recent studies comprising sterol-deficient mutants demonstrated the importance of correct sterol composition and endocytosis for proper membrane compartmentalization.

ENHANCED DISEASE SUSCEPTIBILITY 1 (EDS1) and its interacting partner, PHYTOALEXIN DEFICIENT 4 (PAD4), constitute a regulatory hub that is essential for basal resistance to invasive biotrophic and hemi-biotrophic pathogens. EDS1 and PAD4 are also recruited by Toll-Interleukin-1 receptor (TIR)-type nucleotide binding-leucine rich repeat (NB-LRR) proteins to signal isolate-specific pathogen recognition. Recent work points to a fundamental role of EDS1 and PAD4 in transducing redox signals in response to certain biotic and abiotic stresses. These intracellular proteins are important activators of salicylic acid (SA) signaling and also mediate antagonism between the jasmonic acid (JA) and ethylene (ET) defense response pathways. EDS1 forms several molecularly and spatially distinct complexes with PAD4 and a newly discovered in vivo signaling partner, SENESCENCE ASSOCIATED GENE 101 (SAG101). Together, EDS1, PAD4 and SAG101 provide a major barrier to infection by both host-adapted and non-host pathogens.

WRKY proteins comprise a large family of transcription factors. Despite their dramatic diversification in plants, WRKY genes seem to have originated in early eukaryotes. The cognate DNA-binding site of WRKY factors is well defined, but determining the roles of individual family members in regulating specific transcriptional programs during development or in response to environmental signals remains daunting. This review summarises the recent advances made in starting to unravel the various functions controlled by WRKY proteins.

New findings challenge the traditional view of the plant cell wall as passive structural barrier to invasion by fungal microorganisms. A surveillance system for cell wall integrity appears to sense perturbation of the cell wall structure upon fungal attack and is interconnected with known plant defence signalling pathways. Biotrophic fungi might manipulate this surveillance system for the establishment of biotrophy. The attempts of fungi to invade also induce a sub-cellular polarisation in attacked cells, which activates an ancient vesicle-associated resistance response that possibly enables the focal transport of regulatory cargo and the secretion of toxic cargo. The underlying resistance machinery might have been subverted by biotrophic fungi for pathogenesis.

The apparent under-representation of the term 'plant disease susceptibility' as opposed to 'plant disease resistance' in the current scientific literature might indicate that 'compatibility' has not gained the same appreciation as 'resistance' in the past. However, these seemingly contrary phenomena are intimately linked, and progress in understanding one process inherently contributes to our comprehension of the other. Recent progress in analyzing plant-biotroph compatibility includes the molecular isolation and functional characterization of haustorium-specific cDNAs that encode presumptive hexose- and amino-acid-transporter proteins for proton-driven nutrient uptake. Accumulating evidence from cytological, pharmacological, phytopathological and molecular studies indicates that pathogens mediate the suppression of host defenses in a range of plant-biotroph interactions. Arabidopsis thaliana mutants that are resistant to powdery or downy mildew but that do not exhibit constitutively activated defense could be affected in host-compatibility factors.