Structure-Function Analysis of Barley NLR Immune Receptor MLA10 Reveals Its Cell Compartment Specific Activity in Cell Death and Disease Resistance

Plant intracellular immune receptors comprise a large number of multi-domain proteins resembling animal NOD-like receptors (NLRs). Plant NLRs typically recognize isolate-specific pathogen-derived effectors, encoded by avirulence (AVR) genes, and trigger defense responses often associated with localized host cell death. The barley MLA gene is polymorphic in nature and encodes NLRs of the coiled-coil (CC)-NB-LRR type that each detects a cognate isolate-specific effector of the barley powdery mildew fungus. We report the systematic analyses of MLA10 activity in disease resistance and cell death signaling in barley and Nicotiana benthamiana. MLA10 CC domain-triggered cell death is regulated by highly conserved motifs in the CC and the NB-ARC domains and by the C-terminal LRR of the receptor. Enforced MLA10 subcellular localization, by tagging with a nuclear localization sequence (NLS) or a nuclear export sequence (NES), shows that MLA10 activity in cell death signaling is suppressed in the nucleus but enhanced in the cytoplasm. By contrast, nuclear localized MLA10 is sufficient to mediate disease resistance against powdery mildew fungus. MLA10 retention in the cytoplasm was achieved through attachment of a glucocorticoid receptor hormone-binding domain (GR), by which we reinforced the role of cytoplasmic MLA10 in cell death signaling. Together with our data showing an essential and sufficient nuclear MLA10 activity in disease resistance, this suggests a bifurcation of MLA10-triggered cell death and disease resistance signaling in a compartment-dependent manner

A922 Sequential measurement of 1 hour creatinine clearance (1-CRCL) in critically ill patients at risk of acute kidney injury (AKI)

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Evolution and Conservation of Plant NLR Functions

In plants and animals, nucleotide-binding domain and leucine-rich repeats (NLR)-containing proteins play pivotal roles in innate immunity. Despite their similar biological functions and protein architecture, comparative genome-wide analyses of NLRs and genes encoding NLR-like proteins suggest that plant and animal NLRs have independently arisen in evolution. Furthermore, the demonstration of interfamily transfer of plant NLR functions from their original species to phylogenetically distant species implies evolutionary conservation of the underlying immune principle across plant taxonomy. In this review we discuss plant NLR evolution and summarize recent insights into plant NLR-signaling mechanisms, which might constitute evolutionarily conserved NLR-mediated immune mechanisms

Dying in self-defence: a comparative overview of immunogenic cell death signalling in animals and plants

Host organisms utilise a range of genetically encoded cell death programmes in response to pathogen challenge. Host cell death can restrict pathogen proliferation by depleting their replicative niche and at the same time dying cells can alert neighbouring cells to prepare environmental conditions favouring future pathogen attacks. As expected, many pathogenic microbes have strategies to subvert host cell death to promote their virulence. The structural and lifestyle differences between animals and plants have been anticipated to shape very different host defence mechanisms. However, an emerging body of evidence indicates that several components of the host-pathogen interaction machinery are shared between the two major branches of eukaryotic life. Many proteins involved in cell death execution or cell death-associated immunity in plants and animals exert direct effects on endomembrane and loss of membrane integrity has been proposed to explain the potential immunogenicity of dying cells. In this review we aim to provide a comparative view on how cell death processes are linked to anti-microbial defence mechanisms in plants and animals and how pathogens interfere with these cell death programmes. In comparison to the several well-defined cell death programmes in animals, immunogenic cell death in plant defence is broadly defined as the hypersensitive response. Our comparative overview may help discerning whether specific types of immunogenic cell death exist in plants, and correspondingly, it may provide new hints for previously undiscovered cell death mechanism in animals.This work was supported by the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation, SFB-1403–414786233 to T.M. and H.K.), a grant from the University of Cologne Centre of Excellence in Plant Sciences (T.M.). Research at CRAG was funded with grant PID2019-108595RB-I00 funded by MCIN/AEI/10.13039/501100011033 and through the “Severo Ochoa Programme for Centres of Excellence in R&D” (CEX2019-000902-S funded by MCIN/AEI/10.13039/501100011033) and by the CERCA Programme / Generalitat de Catalunya. Open Access funding enabled and organized by Projekt DEAL.With funding from the Spanish government through the ‘Severo Ochoa Centre of Excellence’ accreditation (CEX2019-000902-S)Peer reviewe

NLR functions in plant and animal immune systems: so far and yet so close

In plants and animals, the NLR family of receptors perceives non-self and modified-self molecules inside host cells and mediates innate immune responses to microbial pathogens. Despite their similar biological functions and protein architecture, animal NLRs are normally activated by conserved microbe-or damage-associated molecular patterns, whereas plant NLRs typically detect strain-specific pathogen effectors. Plant NLRs recognize either the effector structure or effector-mediated modifications of host proteins. The latter indirect mechanism for the perception of non-self, as well as the within-species diversification of plant NLRs, maximize the capacity to recognize non-self through the use of a finite number of innate immunoreceptors. We discuss recent insights into NLR activation, signal initiation through the homotypic association of N-terminal domains and subcellular receptor dynamics in plants and compare those with NLR functions in animals

Dying in self-defence: a comparative overview of immunogenic cell death signalling in animals and plants

Host organisms utilise a range of genetically encoded cell death programmes in response to pathogen challenge. Host cell death can restrict pathogen proliferation by depleting their replicative niche and at the same time dying cells can alert neighbouring cells to prepare environmental conditions favouring future pathogen attacks. As expected, many pathogenic microbes have strategies to subvert host cell death to promote their virulence. The structural and lifestyle differences between animals and plants have been anticipated to shape very different host defence mechanisms. However, an emerging body of evidence indicates that several components of the host-pathogen interaction machinery are shared between the two major branches of eukaryotic life. Many proteins involved in cell death execution or cell death-associated immunity in plants and animals exert direct effects on endomembrane and loss of membrane integrity has been proposed to explain the potential immunogenicity of dying cells. In this review we aim to provide a comparative view on how cell death processes are linked to anti-microbial defence mechanisms in plants and animals and how pathogens interfere with these cell death programmes. In comparison to the several well-defined cell death programmes in animals, immunogenic cell death in plant defence is broadly defined as the hypersensitive response. Our comparative overview may help discerning whether specific types of immunogenic cell death exist in plants, and correspondingly, it may provide new hints for previously undiscovered cell death mechanism in animals

Signatures of host specialization and a recent transposable element burst in the dynamic one-speed genome of the fungal barley powdery mildew pathogen

Background Powdery mildews are biotrophic pathogenic fungi infecting a number of economically important plants. The grass powdery mildew, Blumeria graminis, has become a model organism to study host specialization of obligate biotrophic fungal pathogens. We resolved the large-scale genomic architecture of B. graminis forma specialis hordei (Bgh) to explore the potential influence of its genome organization on the co-evolutionary process with its host plant, barley (Hordeum vulgare). Results The near-chromosome level assemblies of the Bgh reference isolate DH14 and one of the most diversified isolates, RACE1, enabled a comparative analysis of these haploid genomes, which are highly enriched with transposable elements (TEs). We found largely retained genome synteny and gene repertoires, yet detected copy number variation (CNV) of secretion signal peptide-containing protein-coding genes (SPs) and locally disrupted synteny blocks. Genes coding for sequence-related SPs are often locally clustered, but neither the SPs nor the TEs reside preferentially in genomic regions with unique features. Extended comparative analysis with different host-specific B. graminis formae speciales revealed the existence of a core suite of SPs, but also isolate-specific SP sets as well as congruence of SP CNV and phylogenetic relationship. We further detected evidence for a recent, lineage-specific expansion of TEs in the Bgh genome. Conclusions The characteristics of the Bgh genome (largely retained synteny, CNV of SP genes, recently proliferated TEs and a lack of significant compartmentalization) are consistent with a “one-speed” genome that differs in its architecture and (co-)evolutionary pattern from the “two-speed” genomes reported for several other filamentous phytopathogens