Browsing by Subject "Salicylic Acid"
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Item Open Access A genetic screen reveals Arabidopsis stomatal and/or apoplastic defenses against Pseudomonas syringae pv. tomato DC3000.(PLoS pathogens, 2011-10-06) Zeng, Weiqing; Brutus, Alexandre; Kremer, James M; Withers, John C; Gao, Xiaoli; Jones, A Daniel; He, Sheng YangBacterial infection of plants often begins with colonization of the plant surface, followed by entry into the plant through wounds and natural openings (such as stomata), multiplication in the intercellular space (apoplast) of the infected tissues, and dissemination of bacteria to other plants. Historically, most studies assess bacterial infection based on final outcomes of disease and/or pathogen growth using whole infected tissues; few studies have genetically distinguished the contribution of different host cell types in response to an infection. The phytotoxin coronatine (COR) is produced by several pathovars of Pseudomonas syringae. COR-deficient mutants of P. s. tomato (Pst) DC3000 are severely compromised in virulence, especially when inoculated onto the plant surface. We report here a genetic screen to identify Arabidopsis mutants that could rescue the virulence of COR-deficient mutant bacteria. Among the susceptible to coronatine-deficient Pst DC3000 (scord) mutants were two that were defective in stomatal closure response, two that were defective in apoplast defense, and four that were defective in both stomatal and apoplast defense. Isolation of these three classes of mutants suggests that stomatal and apoplastic defenses are integrated in plants, but are genetically separable, and that COR is important for Pst DC3000 to overcome both stomatal guard cell- and apoplastic mesophyll cell-based defenses. Of the six mutants defective in bacterium-triggered stomatal closure, three are defective in salicylic acid (SA)-induced stomatal closure, but exhibit normal stomatal closure in response to abscisic acid (ABA), and scord7 is compromised in both SA- and ABA-induced stomatal closure. We have cloned SCORD3, which is required for salicylic acid (SA) biosynthesis, and SCORD5, which encodes an ATP-binding cassette (ABC) protein, AtGCN20/AtABCF3, predicted to be involved in stress-associated protein translation control. Identification of SCORD5 begins to implicate an important role of stress-associated protein translation in stomatal guard cell signaling in response to microbe-associated molecular patterns and bacterial infection.Item Open Access Dual impact of elevated temperature on plant defence and bacterial virulence in Arabidopsis.(Nature communications, 2017-11-27) Huot, Bethany; Castroverde, Christian Danve M; Velásquez, André C; Hubbard, Emily; Pulman, Jane A; Yao, Jian; Childs, Kevin L; Tsuda, Kenichi; Montgomery, Beronda L; He, Sheng YangEnvironmental conditions profoundly affect plant disease development; however, the underlying molecular bases are not well understood. Here we show that elevated temperature significantly increases the susceptibility of Arabidopsis to Pseudomonas syringae pv. tomato (Pst) DC3000 independently of the phyB/PIF thermosensing pathway. Instead, elevated temperature promotes translocation of bacterial effector proteins into plant cells and causes a loss of ICS1-mediated salicylic acid (SA) biosynthesis. Global transcriptome analysis reveals a major temperature-sensitive node of SA signalling, impacting ~60% of benzothiadiazole (BTH)-regulated genes, including ICS1 and the canonical SA marker gene, PR1. Remarkably, BTH can effectively protect Arabidopsis against Pst DC3000 infection at elevated temperature despite the lack of ICS1 and PR1 expression. Our results highlight the broad impact of a major climate condition on the enigmatic molecular interplay between temperature, SA defence and function of a central bacterial virulence system in the context of a widely studied susceptible plant-pathogen interaction.Item Embargo Next-Generation Mapping of the Salicylic Acid Signaling Hub and Transcriptional Cascade(2024) Powers, Jordan JohnFor over 60 years, salicylic acid (SA) has been known as a key signaling molecule for local and systemic immunity. SA causes drastic cellular reprogramming in a phenomenon known as Systemic Acquired Resistance (SAR). During SAR, thousands of genes transcriptional respond. This transcriptional response is regulated by the cofactor NONEXPRESSER OF PR1 (NPR1), despite NPR1 not having a DNA binding domain. With no DNA binding domain, how this cofactor functions in this transcriptional reprogramming became a question at the forefront of the field. Despite decades of investigation, we have only superficially understood its function, largely due to the reliance on marker genes and low-throughput, molecular biology approaches. While higher throughput methodologies have been employed in previous attempts to identify NPR1 partners and target genes, all efforts yielded futile results. However, with the development of new targeted proteomic techniques and higher signal chromatin profiling techniques, we are poised to adapt these technologies to identify NPR1 proximal proteins and direct targets. Utilizing TurboID, we identified 234 NPR1 proximal partner proteins, including most known NPR1 interactors, validating our methodology. These proximal proteins are enriched with chromatin remodelers, splicing machinery, the Mediator complex, and transcriptional regulators. Strikingly these proximal partners can play either a positive or negative role in establishing SAR. Beyond NPR1 partners, we identified NPR1 target genes upon SA treatment using greenCUT&RUN. Despite a proposed transcription factor switching model, our time course greenCUT&RUN showed NPR1 binds consistently to the same loci after SA treatment through TGA transcription factors and induces a transcriptional cascade comprised of WRKY, NAC, ERF, and MYB transcription factors. This induction requires the condensate formation of NPR1 to stabilize the NPR1 TGA interaction. Through this induced cascade, WRKYs continue propagating this SA transcriptional reprogramming and activating many signaling kinases and defense genes. Beyond NPR1, many conical ideas about transcription induction seem to be amiss in SA-induced genes, including increased chromatin accessibility and histone acetylation, leading rise to the new yet old question; how does NPR1, and the subsequent SA-induce transcription factors, cause this transcriptional reprogramming?
Item Open Access Oxicam-type non-steroidal anti-inflammatory drugs inhibit NPR1-mediated salicylic acid pathway.(Nature communications, 2021-12) Ishihama, Nobuaki; Choi, Seung-Won; Noutoshi, Yoshiteru; Saska, Ivana; Asai, Shuta; Takizawa, Kaori; He, Sheng Yang; Osada, Hiroyuki; Shirasu, KenNonsteroidal anti-inflammatory drugs (NSAIDs), including salicylic acid (SA), target mammalian cyclooxygenases. In plants, SA is a defense hormone that regulates NON-EXPRESSOR OF PATHOGENESIS RELATED GENES 1 (NPR1), the master transcriptional regulator of immunity-related genes. We identify that the oxicam-type NSAIDs tenoxicam (TNX), meloxicam, and piroxicam, but not other types of NSAIDs, exhibit an inhibitory effect on immunity to bacteria and SA-dependent plant immune response. TNX treatment decreases NPR1 levels, independently from the proposed SA receptors NPR3 and NPR4. Instead, TNX induces oxidation of cytosolic redox status, which is also affected by SA and regulates NPR1 homeostasis. A cysteine labeling assay reveals that cysteine residues in NPR1 can be oxidized in vitro, leading to disulfide-bridged oligomerization of NPR1, but not in vivo regardless of SA or TNX treatment. Therefore, this study indicates that oxicam inhibits NPR1-mediated SA signaling without affecting the redox status of NPR1.Item Open Access Redox rhythm reinforces the circadian clock to gate immune response.(Nature, 2015-07-23) Zhou, M; Wang, W; Karapetyan, S; Mwimba, M; Marques, J; Buchler, NE; Dong, XRecent studies have shown that in addition to the transcriptional circadian clock, many organisms, including Arabidopsis, have a circadian redox rhythm driven by the organism's metabolic activities. It has been hypothesized that the redox rhythm is linked to the circadian clock, but the mechanism and the biological significance of this link have only begun to be investigated. Here we report that the master immune regulator NPR1 (non-expressor of pathogenesis-related gene 1) of Arabidopsis is a sensor of the plant's redox state and regulates transcription of core circadian clock genes even in the absence of pathogen challenge. Surprisingly, acute perturbation in the redox status triggered by the immune signal salicylic acid does not compromise the circadian clock but rather leads to its reinforcement. Mathematical modelling and subsequent experiments show that NPR1 reinforces the circadian clock without changing the period by regulating both the morning and the evening clock genes. This balanced network architecture helps plants gate their immune responses towards the morning and minimize costs on growth at night. Our study demonstrates how a sensitive redox rhythm interacts with a robust circadian clock to ensure proper responsiveness to environmental stimuli without compromising fitness of the organism.Item Open Access Salicylic acid biosynthesis is enhanced and contributes to increased biotrophic pathogen resistance in Arabidopsis hybrids.(Nat Commun, 2015-06-12) Yang, Li; Li, Bosheng; Zheng, Xiao-yu; Li, Jigang; Yang, Mei; Dong, Xinnian; He, Guangming; An, Chengcai; Deng, Xing WangHeterosis, the phenotypic superiority of a hybrid over its parents, has been demonstrated for many traits in Arabidopsis thaliana, but its effect on defence remains largely unexplored. Here, we show that hybrids between some A. thaliana accessions show increased resistance to the biotrophic bacterial pathogen Pseudomonas syringae pv. tomato (Pst) DC3000. Comparisons of transcriptomes between these hybrids and their parents after inoculation reveal that several key salicylic acid (SA) biosynthesis genes are significantly upregulated in hybrids. Moreover, SA levels are higher in hybrids than in either parent. Increased resistance to Pst DC3000 is significantly compromised in hybrids of pad4 mutants in which the SA biosynthesis pathway is blocked. Finally, increased histone H3 acetylation of key SA biosynthesis genes correlates with their upregulation in infected hybrids. Our data demonstrate that enhanced activation of SA biosynthesis in A. thaliana hybrids may contribute to their increased resistance to a biotrophic bacterial pathogen.Item Open Access Salicylic acid receptors activate jasmonic acid signalling through a non-canonical pathway to promote effector-triggered immunity.(Nature communications, 2016-10-11) Liu, Lijing; Sonbol, Fathi-Mohamed; Huot, Bethany; Gu, Yangnan; Withers, John; Mwimba, Musoki; Yao, Jian; He, Sheng Yang; Dong, XinnianIt is an apparent conundrum how plants evolved effector-triggered immunity (ETI), involving programmed cell death (PCD), as a major defence mechanism against biotrophic pathogens, because ETI-associated PCD could leave them vulnerable to necrotrophic pathogens that thrive on dead host cells. Interestingly, during ETI, the normally antagonistic defence hormones, salicylic acid (SA) and jasmonic acid (JA) associated with defence against biotrophs and necrotrophs respectively, both accumulate to high levels. In this study, we made the surprising finding that JA is a positive regulator of RPS2-mediated ETI. Early induction of JA-responsive genes and de novo JA synthesis following SA accumulation is activated through the SA receptors NPR3 and NPR4, instead of the JA receptor COI1. We provide evidence that NPR3 and NPR4 may mediate this effect by promoting degradation of the JA transcriptional repressor JAZs. This unique interplay between SA and JA offers a possible explanation of how plants can mount defence against a biotrophic pathogen without becoming vulnerable to necrotrophic pathogens.