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Plant pathogens pose a high risk of yield losses and threaten food security. Technological and scientific advances have improved our understanding of the molecular processes underlying host–pathogen interactions, which paves the way for new strategies in crop disease management beyond the limits of conventional breeding. Cross‐family transfer of immune receptor genes is one such strategy that takes advantage of common plant immune signalling pathways to improve disease resistance in crops. Sensing of microbe‐ or host damage‐associated molecular patterns (MAMPs/DAMPs) by plasma membrane‐resident pattern recognition receptors (PRR) activates pattern‐triggered immunity (PTI) and restricts the spread of a broad spectrum of pathogens in the host plant. In the model plant Arabidopsis thaliana, the S‐domain receptor‐like kinase LIPOOLIGOSACCHARIDE‐SPECIFIC REDUCED ELICITATION (AtLORE, SD1‐29) functions as a PRR, which senses medium‐chain‐length 3‐hydroxylated fatty acids (mc‐3‐OH‐FAs), such as 3‐OH‐C10:0, and 3‐hydroxyalkanoates (HAAs) of microbial origin to activate PTI. In this study, we show that ectopic expression of the Brassicaceae‐specific PRR AtLORE in the solanaceous crop species Solanum lycopersicum leads to the gain of 3‐OH‐C10:0 immune sensing without altering plant development. AtLORE‐transgenic tomato shows enhanced resistance against Pseudomonas syringae pv. tomato DC3000 and Alternaria solani NL03003. Applying 3‐OH‐C10:0 to the soil before infection induces resistance against the oomycete pathogen Phytophthora infestans Pi100 and further enhances resistance to A. solani NL03003. Our study proposes a potential application of AtLORE‐transgenic crop plants and mc‐3‐OH‐FAs as resistance‐inducing biostimulants in disease management. [ABSTRACT FROM AUTHOR]

Summary: Fusarium spp. cause severe economic damage in many crops, exemplified by Panama disease of banana or Fusarium head blight of wheat. Plants sense immunogenic patterns (termed elicitors) at the cell surface to initiate pattern‐triggered immunity (PTI). Knowledge of fungal elicitors and corresponding plant immune‐signaling is incomplete but could yield valuable sources of resistance.We characterized Arabidopsis thaliana PTI responses to a peptide elicitor fraction present in several Fusarium spp. and employed a forward‐genetic screen using plants containing a cytosolic calcium reporter to isolate fusarium elicitor reduced elicitation (fere) mutants.We mapped the causal mutation in fere1 to the leucine‐rich repeat receptor‐like kinase MDIS1‐INTERACTING RECEPTOR‐LIKE KINASE 2 (MIK2) and confirmed a crucial role of MIK2 in fungal elicitor perception. MIK2‐dependent elicitor responses depend on known signaling components and transfer of AtMIK2 is sufficient to confer elicitor sensitivity to Nicotiana benthamiana.Arabidopsis senses Fusarium elicitors by a novel receptor complex at the cell surface that feeds into common PTI pathways. These data increase mechanistic understanding of PTI to Fusarium and place MIK2 at a central position in Arabidopsis elicitor responses. [ABSTRACT FROM AUTHOR]

Changes in cellular calcium levels are one of the earliest signalling events in plants exposed to pathogens or other exogenous factors. In a genetic screen, we identified an Arabidopsis thaliana 'changed calcium elevation 1' (cce1) mutant with attenuated calcium response to the bacterial flagellin flg22 peptide and several other elicitors. Whole‐genome resequencing revealed a mutation in asparagine‐linked glycosylation 12 that encodes the mannosyltransferase responsible for adding the eighth mannose residue in an α‐1,6 linkage to the dolichol‐PP‐oligosaccharide N‐glycosylation glycan tree precursors. While properly targeted to the plasma membrane, misglycosylation of several receptors in the cce1 background suggests that N‐glycosylation is required for proper functioning of client proteins. [ABSTRACT FROM AUTHOR]

Ca2+ is a ubiquitous second messenger for cellular signalling in various stresses and developmental processes. Here, we summarize current developments in the roles of Ca2+ during plant immunity responses. We discuss the early perception events preceding and necessary for triggering cellular Ca2+ fluxes, the potential Ca2+-permeable channels, the decoding of Ca2+ signals predominantly via Ca2+-dependent phosphorylation events and transcriptional reprogramming. To highlight the complexity of the cellular signal network, we briefly touch on the interplay between Ca2+-dependent signalling and selected major signalling mechanisms - with special emphasis on reactive oxygen species at local and systemic levels. [ABSTRACT FROM AUTHOR]

The putative two-pore Ca2+ channel TPC1 has been suggested to be involved in responses to abiotic and biotic stresses. We show that AtTPC1 co-localizes with the K+-selective channel AtTPK1 in the vacuolar membrane. Loss of AtTPC1 abolished Ca2+-activated slow vacuolar (SV) currents, which were increased in AtTPC1-over-expressing Arabidopsis compared to the wild-type. A Ca2+-insensitive vacuolar cation channel, as yet uncharacterized, could be resolved in tpc1-2 knockout plants. The kinetics of ABA- and CO2-induced stomatal closure were similar in wild-type and tpc1-2 knockout plants, excluding a role of SV channels in guard-cell signalling in response to these physiological stimuli. ABA-, K+-, and Ca2+-dependent root growth phenotypes were not changed in tpc1-2 compared to wild-type plants. Given the permeability of SV channels to mono- and divalent cations, the question arises as to whether TPC1 in vivo represents a pathway for Ca2+ entry into the cytosol. Ca2+ responses as measured in aequorin-expressing wild-type, tpc1-2 knockout and TPC1-over-expressing plants disprove a contribution of TPC1 to any of the stimulus-induced Ca2+ signals tested, including abiotic stresses (cold, hyperosmotic, salt and oxidative), elevation in extracellular Ca2+ concentration and biotic factors (elf18, flg22). In good agreement, stimulus- and Ca2+-dependent gene activation was not affected by alterations in TPC1 expression. Together with our finding that the loss of TPC1 did not change the activity of hyperpolarization-activated Ca2+-permeable channels in the plasma membrane, we conclude that TPC1, under physiological conditions, functions as a vacuolar cation channel without a major impact on cytosolic Ca2+ homeostasis. [ABSTRACT FROM AUTHOR]