Publications by authors named "Laurent Zimmerli"

Upon recognition of microbes, pattern recognition receptors (PRRs) activate pattern-triggered immunity. FLAGELLIN SENSING2 (FLS2) and BRASSINOSTEROID INSENSITIVE1-ASSOCIATED KINASE1 (BAK1) form a typical PRR complex that senses bacteria. Here, we report that the kinase activity of the malectin-like receptor-like kinase STRESS INDUCED FACTOR 2 (SIF2) is critical for Arabidopsis () resistance to bacteria by regulating stomatal immunity.

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Epigenetic modifications involve complex and sophisticated control over chromatin states and DNA methylation patterns, which are important for stress tolerance in plants. While the identification of epigenetic modulating enzymes keeps growing, such as , for CG methylation; , , for CHH methylation; and , for CHG methylation; the molecular roles of these regulators in specific physiological functions remain obscure. In a mutant screen, we identified as a new player in plant immunity.

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Recognition of microbe-associated molecular patterns (MAMPs) derived from invading pathogens by plant pattern recognition receptors (PRRs) initiates a subset of defense responses known as pattern-triggered immunity (PTI). Transcription factors (TFs) orchestrate the onset of PTI through complex signaling networks. Here, we characterized the function of ERF19, a member of the Arabidopsis thaliana ethylene response factor (ERF) family.

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Stomatal immunity restricts bacterial entry to leaves through the recognition of microbe-associated molecular patterns (MAMPs) by pattern-recognition receptors (PRRs) and downstream abscisic acid and salicylic acid signaling. Through a reverse genetics approach, we characterized the function of the L-type lectin receptor kinase-V.2 (LecRK-V.

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Proper stomatal responses are essential for plant function in an altered environment. The core signaling pathway for abscisic acid (ABA)-induced stomatal closure involves perception of the hormone that leads to the activation of guard cell anion channels by the protein kinase OPEN STOMATA1. Several other regulators are suggested to modulate the ABA signaling pathway, including the protein ENHANCED RESPONSE TO ABA1 (ERA1), that encodes the farnesyl transferase β-subunit.

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Article Synopsis
  • Plasma membrane-localized pattern recognition receptors (PRRs) like FLS2, EFR, and CERK1 detect microbe-associated molecular patterns (MAMPs) and trigger pattern-triggered immunity (PTI) in plants.
  • A study identified IOS1 as a key player in PTI, demonstrating that Arabidopsis ios1 mutants are more susceptible to bacterial infections due to impaired PTI responses.
  • IOS1 interacts with various PRRs and positively influences their signaling pathways, highlighting its role in enhancing plant immunity against pathogens.
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Pathogen attack leads to transcriptional changes and metabolic modifications allowing the establishment of appropriate plant defences. Transcription factors (TFs) are key players in plant innate immunity. Notably, ethylene response factor (ERF) TFs are integrators of hormonal pathways and are directly responsible for the transcriptional regulation of several jasmonate (JA)/ethylene (ET)-responsive defence genes.

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The ERF (ethylene responsive factor) family is composed of transcription factors (TFs) that are critical for appropriate Arabidopsis thaliana responses to biotic and abiotic stresses. Here we identified and characterized a member of the ERF TF group IX, namely ERF96, that when overexpressed enhances Arabidopsis resistance to necrotrophic pathogens such as the fungus Botrytis cinerea and the bacterium Pectobacterium carotovorum. ERF96 is jasmonate (JA) and ethylene (ET) responsive and ERF96 transcripts accumulation was abolished in JA-insensitive coi1-16 and in ET-insensitive ein2-1 mutants.

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Upon recognition of microbe-associated molecular patterns (MAMPs) such as the bacterial flagellin (or the derived peptide flg22) by pattern-recognition receptors (PRRs) such as the FLAGELLIN SENSING2 (FLS2), plants activate the pattern-triggered immunity (PTI) response. The L-type lectin receptor kinase-VI.2 (LecRK-VI.

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Plants are constantly exposed to potentially pathogenic microbes present in their surrounding environment. Due to the activation of the pattern-triggered immunity (PTI) response that largely relies on accurate detection of pathogen- or microbe-associated molecular patterns by pattern-recognition receptors (PRRs), plants are resistant to the majority of potential pathogens. However, adapted pathogens may avoid recognition or repress plant PTI and resulting diseases significantly affect crop yield worldwide.

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Plasma membrane-localized pattern recognition receptors such as FLAGELLIN SENSING2 (FLS2) and EF-TU RECEPTOR (EFR) recognize microbe-associated molecular patterns (MAMPs) to activate the first layer of plant immunity termed pattern-triggered immunity (PTI). A reverse genetics approach with genes responsive to the priming agent β-aminobutyric acid (BABA) revealed IMPAIRED OOMYCETE SUSCEPTIBILITY1 (IOS1) as a critical PTI player. Arabidopsis thaliana ios1 mutants were hypersusceptible to Pseudomonas syringae bacteria.

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In nature, plants are exposed to a fluctuating environment, and individuals exposed to contrasting environmental factors develop different environmental histories. Whether different environmental histories alter plant responses to a current stress remains elusive. Here, we show that environmental history modulates the plant response to microbial pathogens.

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Pattern-triggered immunity (PTI) is broad spectrum and manipulation of PTI is believed to represent an attractive way to engineer plants with broad-spectrum disease resistance. PTI is activated upon perception of microbe-associated molecular patterns (MAMPs) by pattern-recognition receptors (PRRs). We have recently demonstrated that the L-type lectin receptor kinase-VI.

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A key feature of innate immunity is the ability to recognize and respond to potential pathogens in a highly sensitive and specific manner. In plants, the first layer of defense is induced after recognition by pattern recognition receptors of microbe-associated molecular patterns. This recognition elicits a defense program known as pattern-triggered immunity.

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Sensing of microbial pathogens by pathogen-associated molecular patterns (PAMPs) through pattern recognition receptors (PRRs) elicits a defense program known as PAMP-triggered immunity (PTI). Recently, we have shown that the Arabidopsis thaliana L-TYPE LECTIN RECEPTOR KINASE-VI.2 (LecRK-VI.

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Boosted responsiveness of plant cells to stress at the onset of pathogen- or chemically induced resistance is called priming. The chemical β-aminobutyric acid (BABA) enhances Arabidopsis thaliana resistance to hemibiotrophic bacteria through the priming of the salicylic acid (SA) defence response. Whether BABA increases Arabidopsis resistance to the necrotrophic bacterium Pectobacterium carotovorum ssp.

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Plant stomata function in disease resistance by restricting bacteria entry inside leaves. During plant-bacteria interactions, stomatal closure is initiated by the recognition of Microbe-Associated Molecular Patterns (MAMPs). Recently, we have shown that the Lectin Receptor Kinase V.

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Plant cells can be sensitized toward a subsequent pathogen attack by avirulent pathogens or by chemicals such as β-aminobutyric acid (BABA). This process is called priming. Using a reverse genetic approach in Arabidopsis thaliana, we demonstrate that the BABA-responsive L-type lectin receptor kinase-VI.

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Stomata play an important role in plant innate immunity by limiting pathogen entry into leaves but molecular mechanisms regulating stomatal closure upon pathogen perception are not well understood. Here we show that the Arabidopsis thaliana L-type lectin receptor kinase-V.5 (LecRK-V.

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Sensing environmental changes and initiating a gene expression response are important for plants as sessile autotrophs. The ability of epigenetic status to alter rapidly and reversibly could be a key component to the flexibility of plant responses to the environment. The involvement of epigenetic mechanisms in the response to environmental cues and to different types of abiotic stresses has been documented.

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The priming agent β-aminobutyric acid (BABA) is known to enhance Arabidopsis resistance to the bacterial pathogen Pseudomonas syringae pv. tomato (Pst) DC3000 by potentiating salicylic acid (SA) defence signalling, notably PR1 expression. The molecular mechanisms underlying this phenomenon remain unknown.

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The priming agent beta-aminobutyric acid (BABA) enhances Arabidopsis resistance to microbial pathogens and abiotic stresses through potentiation of the Arabidopsis defense responses. We have previously shown that BABA provokes a stress-induced morphogenic response, reduces vegetative growth and induces accumulation of anthocyanin. It was also found that L-Glutamine restores all tested BABA-induced phenotypes.

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The non-protein amino acid beta-aminobutyric acid (BABA) enhances Arabidopsis resistance to microbial pathogens and abiotic stresses through potentiation of the Arabidopsis defence responses. In this study, it is shown that BABA induces the stress-induced morphogenic response (SIMR). SIMR is observed in plants exposed to sub-lethal stress conditions.

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The non-protein amino acid beta-aminobutyric acid (BABA) primes Arabidopsis to respond more quickly and strongly to pathogen and osmotic stress. Here, we report that BABA also significantly enhances acquired thermotolerance in Arabidopsis. This thermotolerance was dependent on heat shock protein 101, a critical component of the normal heat-shock response.

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Priming: getting ready for battle.

Mol Plant Microbe Interact

October 2006

Infection of plants by necrotizing pathogens or colonization of plant roots with certain beneficial microbes causes the induction of a unique physiological state called "priming." The primed state can also be induced by treatment of plants with various natural and synthetic compounds. Primed plants display either faster, stronger, or both activation of the various cellular defense responses that are induced following attack by either pathogens or insects or in response to abiotic stress.

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