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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. The mutants were hyper-susceptible to hemi-biotrophic bacteria . Accordingly, bacteria-induced up-regulation of , , and defense markers was abolished in mutants. Consistently, at the chromatin level, these defense marker genes showed enrichment of the inactivation mark, H3K9me2; while the activation mark H3K4me3 was reduced in mutants. Immunoprecipitation of associated chromatin further demonstrated that IBM1 binds directly to the gene body of , , and . Taken together, these data suggest that IBM1 plays a critical role in modulating immunity through direct regulation of defense gene expression. Notably, IBM1 maintains a permissive chromatin environment to ensure proper induction of defense genes under some biotic stress.

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. Arabidopsis thaliana plants exposed to repetitive heat, cold, or salt stress were more resistant to virulent bacteria than Arabidopsis grown in a more stable environment. By contrast, long-term exposure to heat, cold, or exposure to high concentrations of NaCI did not provide enhanced protection against bacteria. Enhanced resistance occurred with priming of Arabidopsis patterntriggered immunity (PTI)-responsive genes and the potentiation of PTI-mediated callose deposition. In repetitively stresschallenged Arabidopsis, PTI-responsive genes showed enrichment for epigenetic marks associated with transcriptional activation. Upon bacterial infection, enrichment of RNA polymerase II at primed PTI marker genes was observed in environmentally challenged Arabidopsis. Finally, repetitively stress-challenged historie acetyltransferase1-1 (had-1) mutants failed to demonstrate enhanced resistance to bacteria, priming of PTI, and increased open chromatin states. These findings reveal that environmental history shapes the plant response to bacteria through the development of a HAC1-dependent epigenetic mark characteristic of a primed PTI response, demonstrating a mechanistic link between the primed state in plants and epigenetics.

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 β-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.

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. ERF19 was found to act as a negative regulator of PTI against Botrytis cinerea and Pseudomonas syringae. Notably, overexpression of ERF19 increased plant susceptibility to these pathogens and repressed MAMP-induced PTI outputs. In contrast, expression of the chimeric dominant repressor ERF19–SRDX boosted PTI activation, conferred increased resistance to the fungus B. cinerea, and enhanced elf18-triggered immunity against bacteria. Consistent with a negative role for ERF19 in PTI, MAMP-mediated growth inhibition was weakened or augmented in lines overexpressing ERF19 or expressing ERF19–SRDX, respectively. Using biochemical and genetic approaches, we show that the transcriptional co-repressor Novel INteractor of JAZ (NINJA) associates with and represses the function of ERF19. Our work reveals ERF19 as a novel player in the mitigation of PTI, and highlights a potential role for NINJA in fine-tuning ERF19-mediated regulation of Arabidopsis innate immunity.

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. 2 (LeeRK-VI. 2) contributes to disease resistance against the hemibiotrophic Pseudomonas syringae and the necrotrophic Pectobacterium carotovorum bacteria. Accordingly, LecRK-VI. 2 mRNA levels increased after bacterial inoculation or treatments with microbe-associated molecular patterns (MAMPs). We also show that LecRK-VI. 2 is required for full activation of pattern-triggered immunity (PTI); notably, Iecrk-VL2-1 mutants show reduced upregulation of PTI marker genes, impaired callose deposition, and defective stomatal closure. Overexpression studies combined with genome-wide microarray analyses indicate that LecRK-VI. 2 positively regulates the PTI response. LecRK-VI. 2 is demonstrated to act upstream of mitogen-activated protein kinase signaling, but independently of reactive oxygen production and BOTRYTIS-INDUCED KINASE1 phosphorylation. In addition, complex formation between the MAMP receptor FLAG ELLIN SENSING2 and its signaling partner BRASSINOSTEROID INSENSITIVE1-ASSOCIATED KINASE1 is observed in flg22-treated lecrk-VI. 2-1 mutants. LecRK-VI.2 is also required for full BABA-induced resistance and priming of PTI. Our work identifies LecRK-VI. 2 as a novel mediator of the Arabidopsis PTI response and provides insight into molecular mechanisms governing priming.

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.5) negatively regulates stomatal immunity. Loss of LecRK-V.5 function increased resistance to surface inoculation with virulent bacteria Pseudomonas syringae pv tomato DC3000. Levels of resistance were not affected after infiltration-inoculation, suggesting that LecRK-V.5 functions at an early defense stage. By contrast, lines overexpressing LecRK-V.5 were more susceptible to Pst DC3000. Enhanced resistance in lecrk-V.5 mutants was correlated with constitutive stomatal closure, while increased susceptibility phenotypes in overexpression lines were associated with early stomatal reopening. Lines overexpressing LecRK-V.5 also demonstrated a defective stomatal closure after pathogen-associated molecular pattern (PAMP) treatments. LecRK-V.5 is rapidly expressed in stomatal guard cells after bacterial inoculation or treatment with the bacterial PAMP flagellin. In addition, lecrk-V.5 mutants guard cells exhibited constitutive accumulation of reactive oxygen species (ROS) and inhibition of ROS production opened stomata of lecrk-V.5. LecRK-V.5 is also shown to interfere with abscisic acid-mediated stomatal closure signaling upstream of ROS production. These results provide genetic evidences that LecRK-V.5 negatively regulates stomatal immunity upstream of ROS biosynthesis. Our data reveal that plants have evolved mechanisms to reverse bacteria-mediated stomatal closure to prevent long-term effect on CO(2) uptake and photosynthesis.

Drought and salt stress tolerance of Arabidopsis (Arabidopsis thaliana) plants increased following treatment with the nonprotein amino acid [beta]-aminobutyric acid (BABA), known as an inducer of resistance against infection of plants by numerous pathogens. BABA-pretreated plants showed earlier and higher expression of the salicylic acid-dependent PR-1 and PR-5 and the abscisic acid (ABA)-dependent RAB-18 and RD-29A genes following salt and drought stress. However, non-expressor of pathogenesis-related genes 1 and constitutive expressor of pathogenesis-related genes 1 mutants as well as transgenic NahG plants, all affected in the salicylic acid signal transduction pathway, still showed increased salt and drought tolerance after BABA treatment. On the contrary, the ABA deficient 1 and ABA insensitive 4 mutants, both impaired in the ABA-signaling pathway, could not be protected by BABA application. Our data demonstrate that BABA-induced water stress tolerance is based on enhanced ABA accumulation resulting in accelerated stress gene expression and stomatal closure. Here, we show a possibility to increase plant tolerance for these abiotic stresses through effective priming of the preexisting defense pathways without resorting to genetic alterations.

Summary 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.2) and ‐VII.1 (LecRK‐VII.1). Analyses of interactions with the PRR FLAGELLIN SENSING2 (FLS2) were performed by co‐immunoprecipitation and bimolecular fluorescence complementation and whole‐cell patch‐clamp analyses were used to evaluate guard cell Ca2+‐permeable cation channels. The Arabidopsis thaliana LecRK‐V.2 and LecRK‐VII.1 and notably their kinase activities were required for full activation of stomatal immunity. Knockout lecrk‐V.2 and lecrk‐VII.1 mutants were hyper‐susceptible to Pseudomonas syringae infection and showed defective stomatal closure in response to bacteria or to the MAMPs flagellin and EF‐Tu. By contrast, Arabidopsis over‐expressing LecRK‐V.2 or LecRK‐VII.1 demonstrated a potentiated stomatal immunity. LecRK‐V.2 and LecRK‐VII.1 are shown to be part of the FLS2 PRR complex. In addition, LecRK‐V.2 and LecRK‐VII.1 were critical for methyl jasmonate (MeJA)‐mediated stomatal closure, notably for MeJA‐induced activation of guard cell Ca2+‐permeable cation channels. This study highlights the role of LecRK‐V.2 and LecRK‐VII.1 in stomatal immunity at the FLS2 PRR complex and in MeJA‐mediated stomatal closure.

The nonprotein amino acids γ -aminobutyric acid (GABA) and β -aminobutyric acid (BABA) have known biological effects in animals and plants. Their mode of action has been the object of thorough research in animals but remains unclear in plants. Our objective was to study the mode of action of BABA in the protection of Arabidopis plants against virulent pathogens. BABA protected Arabidopsis against the oomycete pathogen Peronospora parasitica through activation of natural defense mechanisms of the plant such as callose deposition, the hypersensitive response, and the formation of trailing necroses. BABA was still fully protective against P. parasitica in transgenic plants or mutants impaired in the salicylic acid, jasmonic acid, and ethylene signaling pathways. Treatment with BABA did not induce the accumulation of mRNA of the systemic acquired resistance (SAR)-associated PR-1 and the ethylene- and jasmonic acid-dependent PDF1.2 genes. However, BABA potentiated the accumulation of PR-1 mRNA after attack by virulent pathogenic bacteria. As a result, BABA-treated Arabidopsis plants were less diseased compared with the untreated control. In the case of bacteria, BABA protected mutants insensitive to jasmonic acid and ethylene but was not active in plants impaired in the SAR transduction pathway. Thus, BABA protects Arabidopsis against different virulent pathogens by potentiating pathogen-specific plant resistance mechanisms. In addition, we provide evidence that BABA-mediated papilla formation after P. parasitica infection is independent of the SAR signaling pathway.

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. Transcriptional activation or repression by ERFs is achieved through the binding to JA/ET-responsive gene promoters. In this review, we describe the regulation and mode of action at a molecular level of ERFs involved in Arabidopsis thaliana immunity. In particular, we focus on defence activators such as ERF1, ORA59, ERF6, and the recently described ERF96.