Plants sense potential microbial invaders by using patternrecognition receptors to recognize pathogen-associated molecular patterns (PAMPs) 1 . In Arabidopsis thaliana, the leucine-rich repeat receptor kinases flagellin-sensitive 2 (FLS2) (ref.2) and elongation factor Tu receptor (EFR) (ref.3) act as pattern-recognition receptors for the bacterial PAMPs flagellin 4 and elongation factor Tu (EF-Tu) (ref. 5) and contribute to resistance against bacterial pathogens. Little is known about the molecular mechanisms that link receptor activation to intracellular signal transduction. Here we show that BAK1 (BRI1-associated receptor kinase 1), a leucinerich repeat receptor-like kinase that has been reported to regulate the brassinosteroid receptor BRI1 (refs 6,7), is involved in signalling by FLS2 and EFR. Plants carrying bak1 mutations show normal flagellin binding but abnormal early and late flagellintriggered responses, indicating that BAK1 acts as a positive regulator in signalling. The bak1-mutant plants also show a reduction in early, but not late, EF-Tu-triggered responses. The decrease in responses to PAMPs is not due to reduced sensitivity to brassinosteroids. We provide evidence that FLS2 and BAK1 form a complex in vivo, in a specific ligand-dependent manner, within the first minutes of stimulation with flagellin. Thus, BAK1 is not only associated with developmental regulation through the plant hormone receptor BRI1 (refs 6,7), but also has a functional role in PRR-dependent signalling, which initiates innate immunity.PAMPs have key roles as activators of the innate immune response in animals 8 and, analogously, as 'general elicitors' of defence responses in plants [1][2][3][4][5][9][10][11] . We have previously characterized FLS2 and EFR as the pattern-recognition receptors (PRRs) for flagellin (represented by a 22-amino-acid peptide, flg22) and for EF-Tu (represented by the peptides elf18 and elf26, which correspond to its amino terminus), respectively 2-5,10 . Flagellin and EF-Tu rapidly induce a common set of Arabidopsis genes for leucine-rich repeat receptor-like kinases (LRR-RLKs), including FLS2 and EFR themselves 3,11 . This led to the assumption that some of these PAMPinduced LRR-RLKs might encode additional components of PAMP perception or signalling. Using a reverse genetic approach, we tested a collection of insertional mutants in these LRR-RLKs (previously used for identification of the EFR gene 3 ) for responsiveness to flg22 and found that two mutants with insertions in the LRR-RLK gene At4g33430 have reduced sensitivity to flg22 in seedling growth assays (Fig. 1a,b). In more than 10 repetitions of seedling growth assays with these mutants, we always observed a clear reduction (but never a complete loss) of sensitivity to flg22 and flg22-related peptides. By contrast, the mutants seemed to be as sensitive as the wild type to treatment with elf18 in more than five seedling growth assays (Fig. 1b and data not shown).
Innate immunity constitutes the first line of defense against attempted microbial invasion, and it is a well-described phenomenon in vertebrates and insects. Recent pioneering work has revealed striking similarities between the molecular organization of animal and plant systems for nonself recognition and anti-microbial defense. Like animals, plants have acquired the ability to recognize invariant pathogen-associated molecular patterns (PAMPs) that are characteristic of microbial organisms but which are not found in potential host plants. Such structures, also termed general elicitors of plant defense, are often indispensable for the microbial lifestyle and, upon receptor-mediated perception, inevitably betray the invader to the plant's surveillance system. Remarkable similarities have been uncovered in the molecular mode of PAMP perception in animals and plants, including the discovery of plant receptors resembling mammalian Toll-like receptors or cytoplasmic nucleotide-binding oligomerization domain leucine-rich repeat proteins. Moreover, molecular building blocks of PAMP-induced signaling cascades leading to the transcriptional activation of immune response genes are shared among the two kingdoms. In particular, nitric oxide as well as mitogen-activated protein kinase cascades have been implicated in triggering innate immune responses, part of which is the production of antimicrobial compounds. In addition to PAMP-mediated pathogen defense, disease resistance programs are often initiated upon plant-cultivar-specific recognition of microbial race-specific virulence factors, a recognition specificity that is not known from animals.
Plants and animals possess innate immune systems to prevent infections and are effectively "nonhosts" for most potential pathogens. The molecular mechanisms underlying nonhost immunity in plants remain obscure. In Arabidopsis, nonhost/nonpathogenic Pseudomonas syringae sustains but pathogenic P. syringae suppresses early MAMP (microbe-associated molecular pattern) marker-gene activation. We performed a cell-based genetic screen of virulence factors and identified AvrPto and AvrPtoB as potent and unique suppressors of early-defense gene transcription and MAP kinase (MAPK) signaling. Unlike effectors of mammalian pathogens, AvrPto and AvrPtoB intercept multiple MAMP-mediated signaling upstream of MAPKKK at the plasma membrane linked to the receptor. In transgenic Arabidopsis, AvrPto blocks early MAMP signaling and enables nonhost P. syringae growth. Deletions of avrPto and avrPtoB from pathogenic P. syringae reduce its virulence. The studies reveal a fundamental role of MAMP signaling in nonhost immunity, and a novel action of type III effectors from pathogenic bacteria.
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