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Emerging evidence suggests a beneficial role of rhizobacteria in ameliorating plant disease resistance in an environment-friendly way. In this study, we characterize a rhizobacterium, Bacillus cereus NJ01, that enhances bacterial pathogen resistance in rice and Arabidopsis. Transcriptome analyses show that root inoculation of NJ01 induces the expression of salicylic acid (SA)- and abscisic acid (ABA)-related genes in Arabidopsis leaves. Genetic evidence showed that EDS1, PAD4, and WRKY18 are required for B. cereus NJ01-induced bacterial resistance. An EDS1-PAD4 complex interacts with WRKY18 and enhances its DNA binding activity. WRKY18 directly binds to the W box in the promoter region of the SA biosynthesis gene ICS1 and ABA biosynthesis genes NCED3 and NCED5 and contributes to the NJ01-induced bacterial resistance. Taken together, our findings indicate a role of the EDS1/PAD4-WRKY18 complex in rhizobacteria-induced disease resistance., Competing Interests: Declaration of interests The authors declare no competing interests., (Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.)

The phytohormones salicylic acid (SA) and jasmonic acid (JA) are major players in plant immunity. Numerous studies have provided evidence that SA- and JA-mediated signaling interact with each other (SA-JA crosstalk) to orchestrate plant immune responses against pathogens. At the same time, SA-JA crosstalk is often exploited by pathogens to promote their virulence. In this review, we summarize our current knowledge of molecular mechanisms for and modulations of SA-JA crosstalk during pathogen infection., (© 2022 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society.)

The plant immune signaling network needs to be robust against attack from fast-evolving pathogens and tunable to optimize immune responses. We investigated the basis of robustness and tunability in the signaling network controlling pattern-triggered immunity (PTI) in Arabidopsis. A dynamic network model containing four major signaling sectors, the jasmonate, ethylene, phytoalexin-deficient 4, and salicylate sectors, which together govern up to 80% of the PTI levels, was built using data for dynamic sector activities and PTI levels under exhaustive combinatorial sector perturbations. Our regularized multiple regression model had a high level of predictive power and captured known and unexpected signal flows in the network. The sole inhibitory sector in the model, the ethylene sector, contributed centrally to network robustness via its inhibition of the jasmonate sector. The model's multiple input sites linked specific signal input patterns varying in strength and timing to different network response patterns, indicating a mechanism enabling tunability., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Network robustness is a crucial property of the plant immune signaling network because pathogens are under a strong selection pressure to perturb plant network components to dampen plant immune responses. Nevertheless, modulation of network robustness is an area of network biology that has rarely been explored. While two modes of plant immunity, Effector-Triggered Immunity (ETI) and Pattern-Triggered Immunity (PTI), extensively share signaling machinery, the network output is much more robust against perturbations during ETI than PTI, suggesting modulation of network robustness. Here, we report a molecular mechanism underlying the modulation of the network robustness in Arabidopsis thaliana. The salicylic acid (SA) signaling sector regulates a major portion of the plant immune response and is important in immunity against biotrophic and hemibiotrophic pathogens. In Arabidopsis, SA signaling was required for the proper regulation of the vast majority of SA-responsive genes during PTI. However, during ETI, regulation of most SA-responsive genes, including the canonical SA marker gene PR1, could be controlled by SA-independent mechanisms as well as by SA. The activation of the two immune-related MAPKs, MPK3 and MPK6, persisted for several hours during ETI but less than one hour during PTI. Sustained MAPK activation was sufficient to confer SA-independent regulation of most SA-responsive genes. Furthermore, the MPK3 and SA signaling sectors were compensatory to each other for inhibition of bacterial growth as well as for PR1 expression during ETI. These results indicate that the duration of the MAPK activation is a critical determinant for modulation of robustness of the immune signaling network. Our findings with the plant immune signaling network imply that the robustness level of a biological network can be modulated by the activities of network components., Competing Interests: Daisuke Igarashi is employed by Ajinomoto Co., Inc. This does not alter our adherence to all PLoS Genetics policies on sharing data and materials.

Arabidopsis thaliana calmodulin binding protein 60g (CBP60g) contributes to production of salicylic acid (SA) in response to recognition of microbe-associated molecular patterns (MAMPs) such as flg22, a fragment of bacterial flagellin. Calmodulin binding is required for the function of CBP60g in limiting growth of the bacterial pathogen Pseudomonas syringae pv. maculicola (Pma) ES4326 and activation of SA synthesis. Here, we describe a closely related protein, SARD1. Unlike CBP60g, SARD1 does not bind calmodulin. Growth of Pma ES4326 is enhanced in sard1 mutants. In cbp60g sard1 double mutants, growth of Pma ES4326 is greatly enhanced, and SA levels and expression of PR-1 and SID2 are dramatically reduced. Expression profiling placed the CBP60g/SARD1 node between the PAD4/EDS1 and SA nodes in the defense signaling network, and indicated that CBP60g and SARD1 affect defense responses in addition to SA production. A DNA motif bound by CBP60g and SARD1, GAAATTT, was significantly over-represented in promoters of CBP60g/SARD1-dependent genes, suggesting that expression of these genes is modulated by CBP60g/SARD1 binding. Gene expression patterns showed a stronger effect of cbp60g mutations soon after activation of a defense response, and a stronger effect of sard1 mutations at later times. The results are consistent with a model in which CBP60g and SARD1 comprise a partially redundant protein pair that is required for activation of SA production as well as other defense responses, with CBP60g playing a more important role early during the defense response, and SARD1 to playing a more important role later., (© 2011 The Authors. The Plant Journal © 2011 Blackwell Publishing Ltd.)

RNA-binding proteins (RBP) can control gene expression at both transcriptional and post-transcriptional levels. Plants respond to pathogen infection with rapid reprogramming of gene expression. However, little is known about how plant RBP function in plant immunity. Here, we describe the involvement of an RBP, Arabidopsis thaliana RNA-binding protein-defense related 1 (AtRBP-DR1; At4g03110), in resistance to the pathogen Pseudomonas syringae pv. tomato DC3000. AtRBP-DR1 loss-of-function mutants showed enhanced susceptibility to P. syringae pv. tomato DC3000. Overexpression of AtRBP-DR1 led to enhanced resistance to P. syringae pv. tomato DC3000 strains and dwarfism. The hypersensitive response triggered by P. syringae pv. tomato DC3000 avrRpt2 was compromised in the Atrbp-dr1 mutant and enhanced in the AtRBP-DR1 overexpression line at early time points. AtRBP-DR1 overexpression lines showed higher mRNA levels of SID2 and PR1, which are salicylic acid (SA) inducible, as well as spontaneous cell death in mature leaves. Consistent with these observations, the SA level was low in the Atrbp-dr1 mutant but high in the overexpression line. The SA-related phenotype in the overexpression line was fully dependent on SID2. Thus, AtRBP-DR1 is a positive regulator of SA-mediated immunity, possibly acting on SA signaling-related genes at a post-transcriptional level.

Salicylic acid (SA)-induced defense responses are important factors during effector triggered immunity and microbe-associated molecular pattern (MAMP)-induced immunity in plants. This article presents evidence that a member of the Arabidopsis CBP60 gene family, CBP60g, contributes to MAMP-triggered SA accumulation. CBP60g is inducible by both pathogen and MAMP treatments. Pseudomonas syringae growth is enhanced in cbp60g mutants. Expression profiles of a cbp60g mutant after MAMP treatment are similar to those of sid2 and pad4, suggesting a defect in SA signaling. Accordingly, cbp60g mutants accumulate less SA when treated with the MAMP flg22 or a P. syringae hrcC strain that activates MAMP signaling. MAMP-induced production of reactive oxygen species and callose deposition are unaffected in cbp60g mutants. CBP60g is a calmodulin-binding protein with a calmodulin-binding domain located near the N-terminus. Calmodulin binding is dependent on Ca(2+). Mutations in CBP60g that abolish calmodulin binding prevent complementation of the SA production and bacterial growth defects of cbp60g mutants, indicating that calmodulin binding is essential for the function of CBP60g in defense signaling. These studies show that CBP60g constitutes a Ca(2+) link between MAMP recognition and SA accumulation that is important for resistance to P. syringae.

Plants respond to pathogen infection using an innate immune system with at least two distinct recognition mechanisms. One mechanism recognizes microbe-associated molecular patterns (MAMPs). The other is based on resistance (R) genes and specifically recognizes certain pathogen virulence factors, including those delivered through the type III secretion system (TTSS) of bacteria. Salicylic acid (SA)-mediated responses are an important part of the R gene-mediated defense. Substantial overlaps between MAMP-triggered and SA-mediated responses have been reported. However, interactions between MAMP-triggered and SA-mediated signaling mechanisms have not been well documented. Here we report intimate interactions between MAMP-triggered and SA-mediated signaling. We found that SA accumulated at a higher level 6 h after treatment with a MAMP, flg22 or inoculation with Pseudomonas syringae pv. tomato DC3000 (PstDC3000) hrcC mutant, which is deficient in TTSS function. Disruptions of SA signaling components, such as SID2 and PAD4, strongly affected MAMP-triggered responses monitored by expression profiling. We found two groups of genes that were induced by PstDC3000 hrcC in an SA-dependent manner. One group was SID2-dependent at all time points, whereas the other was SID2-independent at early time points and SID2-dependent at later time points. Thus, the expression of the latter genes responds to MAMPs through both SA-independent and SA-dependent signaling mechanisms. Strong resistance to PstDC3000 hrcC was dependent on SA signaling. These results indicate that the SA increase triggered by MAMPs is a major component of the MAMP-triggered signaling mechanism, explaining the overlapping spectra of MAMP-triggered and SA-mediated responses.

Summary: Abiotic and biotic environments influence a myriad of plant‐related processes, including growth, development, and the establishment and maintenance of interaction(s) with microbes. In the case of the latter, elevated temperature has been shown to be a key factor that underpins host resistance and pathogen virulence.In this study, we elucidate a role for Arabidopsis NON‐RACE‐SPECIFIC DISEASE RESISTANCE1 (NDR1) by exploiting effector‐triggered immunity to define the regulation of plant host immunity in response to both pathogen infection and elevated temperature.We generated time‐series RNA sequencing data of WT Col‐0, an NDR1 overexpression line, and ndr1 and ics1‐2 mutant plants under elevated temperature. Not surprisingly, the NDR1‐overexpression line showed genotype‐specific gene expression changes related to defense response and immune system function.The results described herein support a role for NDR1 in maintaining cell signaling during simultaneous exposure to elevated temperature and avirulent pathogen stressors. [ABSTRACT FROM AUTHOR]

Network robustness is a crucial property of the plant immune signaling network because pathogens are under a strong selection pressure to perturb plant network components to dampen plant immune responses. Nevertheless, modulation of network robustness is an area of network biology that has rarely been explored. While two modes of plant immunity, Effector-Triggered Immunity (ETI) and Pattern-Triggered Immunity (PTI), extensively share signaling machinery, the network output is much more robust against perturbations during ETI than PTI, suggesting modulation of network robustness. Here, we report a molecular mechanism underlying the modulation of the network robustness in Arabidopsis thaliana. The salicylic acid (SA) signaling sector regulates a major portion of the plant immune response and is important in immunity against biotrophic and hemibiotrophic pathogens. In Arabidopsis, SA signaling was required for the proper regulation of the vast majority of SA-responsive genes during PTI. However, during ETI, regulation of most SA-responsive genes, including the canonical SA marker gene PR1, could be controlled by SA-independent mechanisms as well as by SA. The activation of the two immune-related MAPKs, MPK3 and MPK6, persisted for several hours during ETI but less than one hour during PTI. Sustained MAPK activation was sufficient to confer SA-independent regulation of most SA-responsive genes. Furthermore, the MPK3 and SA signaling sectors were compensatory to each other for inhibition of bacterial growth as well as for PR1 expression during ETI. These results indicate that the duration of the MAPK activation is a critical determinant for modulation of robustness of the immune signaling network. Our findings with the plant immune signaling network imply that the robustness level of a biological network can be modulated by the activities of network components. [ABSTRACT FROM AUTHOR]

Network robustness is a crucial property of the plant immune signaling network because pathogens are under a strong selection pressure to perturb plant network components to dampen plant immune responses. Nevertheless, modulation of network robustness is an area of network biology that has rarely been explored. While two modes of plant immunity, Effector-Triggered Immunity (ETI) and Pattern-Triggered Immunity (PTI), extensively share signaling machinery, the network output is much more robust against perturbations during ETI than PTI, suggesting modulation of network robustness. Here, we report a molecular mechanism underlying the modulation of the network robustness in Arabidopsis thaliana. The salicylic acid (SA) signaling sector regulates a major portion of the plant immune response and is important in immunity against biotrophic and hemibiotrophic pathogens. In Arabidopsis, SA signaling was required for the proper regulation of the vast majority of SA-responsive genes during PTI. However, during ETI, regulation of most SA-responsive genes, including the canonical SA marker gene PR1, could be controlled by SA-independent mechanisms as well as by SA. The activation of the two immune-related MAPKs, MPK3 and MPK6, persisted for several hours during ETI but less than one hour during PTI. Sustained MAPK activation was sufficient to confer SA-independent regulation of most SA-responsive genes. Furthermore, the MPK3 and SA signaling sectors were compensatory to each other for inhibition of bacterial growth as well as for PR1 expression during ETI. These results indicate that the duration of the MAPK activation is a critical determinant for modulation of robustness of the immune signaling network. Our findings with the plant immune signaling network imply that the robustness level of a biological network can be modulated by the activities of network components. [ABSTRACT FROM AUTHOR]

To better dissect non-host resistance against haustorium-forming powdery mildew pathogens, a sow thistle powdery mildew isolate designated Golovinomyces cichoracearum UMSG1 that has largely overcome penetration resistance but is invariably stopped by post-invasion non-host resistance of Arabidopsis thaliana was identified. The post-invasion non-host resistance is mainly manifested as the formation of a callosic encasement of the haustorial complex (EHC) and hypersensitive response (HR), which appears to be controlled by both salicylic acid (SA)-dependent and SA-independent defence pathways, as supported by the susceptibility of the pad4/sid2 double mutant to the pathogen. While the broad-spectrum resistance protein RPW8.2 enhances post-penetration resistance against G. cichoracearum UCSC1, a well-adapted powdery mildew pathogen, RPW8.2, is dispensable for post-penetration resistance against G. cichoracearum UMSG1, and its specific targeting to the extrahaustorial membrane is physically blocked by the EHC, resulting in HR cell death. Taken together, the present work suggests an evolutionary scenario for the Arabidopsis–powdery mildew interaction: EHC formation is a conserved subcellular defence evolved in plants against haustorial invasion; well-adapted powdery mildew has evolved the ability to suppress EHC formation for parasitic growth and reproduction; RPW8.2 has evolved to enhance EHC formation, thereby conferring haustorium-targeted, broad-spectrum resistance at the post-invasion stage. [ABSTRACT FROM PUBLISHER]

Phytohormones are produced by plants and play central roles in interactions with pathogenic and beneficial microbes as well as plant growth and development. Each phytohormone pathway consists of its biosynthesis, transport, perception, and signaling and is intertwined with each other at various levels to form phytohormone networks in plants. Different kinds of microbes also produce phytohormones that exert physiological roles within microbes and manipulate phytohormone networks in plants by using phytohormones, their mimics, and proteinaceous effectors. In turn, plant-derived phytohormones can directly or indirectly through plant signaling networks affect microbial metabolism and community assembly. Therefore, phytohormone networks in plants and microbes are connected through plant and microbial phytohormones and other molecules to form inter-organismal phytohormone networks. In this review, we summarize recent progress on molecular mechanisms of inter-organismal phytohormone networks and discuss future steps necessary for advancing our understanding of phytohormone networks. [ABSTRACT FROM AUTHOR]

The phytohormone network consisting of jasmonate, ethylene, PHYTOALEXIN-DEFICIENT4, and salicylic acid signaling is required for the two modes of plant immunity, pattern-triggered immunity (PTI), and effector-triggered immunity (ETI). A previous study showed that during PTI, the transcriptional responses of over 5000 genes qualitatively depend on complex interactions between the network components. However, the role of the network in transcriptional reprogramming during ETI and whether it differs between PTI and ETI remain elusive. Here, we generated time-series RNA-sequencing data of Arabidopsis thaliana wild-type and combinatorial mutant plants deficient in components of the network upon challenge with virulent or ETI-triggering avirulent strains of the foliar bacterial pathogen Pseudomonas syringae. Resistant plants such as the wild type achieved high-amplitude transcriptional reprogramming 4 h after challenge with avirulent strains and sustained this transcriptome response. Strikingly, susceptible plants including the quadruple network mutant showed almost identical transcriptome responses to resistant plants but with several hours delay. Furthermore, gene coexpression network structure was highly conserved between the wild type and quadruple mutant. Thus, in contrast to PTI, the phytohormone network is required only for achieving high-amplitude transcriptional reprogramming within the early time window of ETI against this bacterial pathogen. [ABSTRACT FROM AUTHOR]