Plasma membrane-localized pattern recognition receptors (PRRs) such as FLAGELLIN SENSING2 (FLS2), EF-TU RECEPTOR (EFR), and CHITIN ELICITOR RECEPTOR KINASE1 (CERK1) recognize microbe-associated molecular patterns (MAMPs) to activate pattern-triggered immunity (PTI). A reverse genetics approach on genes responsive to the priming agent b-aminobutyric acid (BABA) revealed IMPAIRED OOMYCETE SUSCEPTIBILITY1 (IOS1) as a critical PTI player. Arabidopsis thaliana ios1 mutants were hypersusceptible to Pseudomonas syringae bacteria. Accordingly, ios1 mutants showed defective PTI responses, notably delayed upregulation of the PTI marker gene FLG22-INDUCED RECEPTOR-LIKE KINASE1, reduced callose deposition, and mitogen-activated protein kinase activation upon MAMP treatment. Moreover, Arabidopsis lines overexpressing IOS1 were more resistant to bacteria and showed a primed PTI response. In vitro pull-down, bimolecular fluorescence complementation, coimmunoprecipitation, and mass spectrometry analyses supported the existence of complexes between the membrane-localized IOS1 and BRASSINOSTEROID INSENSITIVE1-ASSOCIATED KINASE1 (BAK1)-dependent PRRs FLS2 and EFR, as well as with the BAK1-independent PRR CERK1. IOS1 also associated with BAK1 in a ligand-independent manner and positively regulated FLS2-BAK1 complex formation upon MAMP treatment. In addition, IOS1 was critical for chitinmediated PTI. Finally, ios1 mutants were defective in BABA-induced resistance and priming. This work reveals IOS1 as a novel regulatory protein of FLS2-, EFR-, and CERK1-mediated signaling pathways that primes PTI activation. INTRODUCTIONPlants possess multilayered recognition systems that detect pathogens at various stages of infection and proliferation. Recognition of microbial invasion is essentially based upon the host's ability to distinguish between self and non-self components. Early microbial pathogens detection is performed by cell surfacelocalized pattern recognition receptors (PRRs) that sense pathogen-or microbe-associated molecular patterns (PAMPs or MAMPs) (Monaghan and Zipfel, 2012). Major examples of MAMPs are lipopolysaccharides present in the envelope of Gram-negative bacteria, eubacterial flagellin, eubacterial elongation factor Tu (EF-Tu), peptidoglycans from Gram-positive bacteria, methylated bacterial DNA fragments, and fungal cell wall-derived chitins (Girardin et al., 2002;Cook et al., 2004;Boller and Felix, 2009). MAMP recognition promptly triggers the activation of patterntriggered immunity (PTI) (Tsuda and Katagiri, 2010). Early PTI responses, such as calcium influx, production of reactive oxygen species (ROS), and activation of mitogen-activated protein (MAP) kinases, induce transcriptional reprogramming mediated by plant WRKY transcription factors as well as calmodulin binding proteins (Boller and Felix, 2009;Tena et al., 2011). In addition, Arabidopsis thaliana plants close stomata in a MAMP-dependent manner when in contact with bacteria (Melotto et al., 2006;Singh et al., 2012). Callose deposition and PTI marker gene up...
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 patterntriggered immunity (PTI). A reverse genetics approach with genes responsive to the priming agent b-aminobutyric acid (BABA) revealed IMPAIRED OOMYCETE SUSCEPTIBILITY1 (IOS1) as a critical PTI player. Arabidopsis thaliana ios1 mutants were hypersusceptible to Pseudomonas syringae bacteria. Accordingly, ios1 mutants demonstrated defective PTI responses, notably delayed upregulation of PTI marker genes, lower callose deposition, and mitogen-activated protein kinase activities upon bacterial infection or MAMP treatment. Moreover, Arabidopsis lines overexpressing IOS1 were more resistant to P. syringae and demonstrated a primed PTI response. In vitro pull-down, bimolecular fluorescence complementation, coimmunoprecipitation, and mass spectrometry analyses supported the existence of complexes between the membranelocalized IOS1 and FLS2 and EFR. IOS1 also associated with BRASSINOSTEROID INSENSITIVE1-ASSOCIATED KINASE1 (BAK1) in a ligand-independent manner and positively regulated FLS2/BAK1 complex formation upon MAMP treatment. Finally, ios1 mutants were defective in BABA-induced resistance and priming. This work reveals IOS1 as a regulatory protein of FLS2-and EFR-mediated signaling that primes PTI activation upon bacterial elicitation.
Selected beta-amino acids, such as beta-aminobutyric acid (BABA) and R-beta-homoserine (RBH), can prime plants for resistance against a broad spectrum of diseases. Here, we describe a genome-wide screen of fully annotated Arabidopsis thaliana T-DNA insertion lines for impaired in RBH-induced immunity (iri) mutants against the downy mildew pathogen Hyaloperonospora arabidopsidis, yielding 104 lines that were partially affected and four lines that were completely impaired in RBH-induced resistance. We confirmed the iri1-1 mutant phenotype with an independent T-DNA insertion line in the same gene, encoding the high-affinity amino acid transporter LYSINE HISTIDINE TRANSPORTER 1 (LHT1). Uptake experiments with yeast cells expressing LHT1 and mass spectrometry-based quantification of RBH and BABA in leaves of lht1 mutant and LHT1 overexpression lines revealed that LHT1 acts as the main transporter for cellular uptake and systemic distribution of RBH and BABA. Subsequent characterization of lht1 mutant and LHT1 overexpression lines for induced resistance and growth responses revealed that the levels of LHT1-mediated uptake determine the trade-off between induced resistance and plant growth by RBH and BABA.
Selected beta-amino acids, such as beta-aminobutyric acid (BABA) and R-beta-homoserine (RBH), can prime plants for broad-spectrum resistance against diseases. Here, we describe a genome-wide screen of fully annotated Arabidopsis T-DNA insertion lines for impairment in RBH-induced immunity against the downy mildew pathogen Hyaloperonospora arabidopsidis, yielding 104 lines that were partially affected and 4 lines that were completely impaired in RBH-induced immunity (iri). The iri1-1 mutant phenotype could be confirmed by an independent T-DNA insertion in the same gene, encoding the high-affinity amino acid transporter LHT1. Using uptake experiments with IRI1/LHT1-expressing yeast cells and mass spectrometry-based quantification of RBH and BABA in leaves of mutant and over-expression lines of IRI1/LHT1, we demonstrate that IRI1/LHT1 acts as the main transporter for cellular uptake and systemic distribution of RBH and BABA. Subsequent characterisation of mutant and over-expression lines of IRI1/LHT1 for induced resistance and growth responses revealed that the level of IRI1/LHT1 expression determines the trade-off between induced resistance and plant growth by RBH and BABA.
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