1,018 research outputs found

    USES OF THE PSEUDOMONAS SYRINGAE EFFECTOR PROTEIN HOPU1 RELATED TO ITSABILITY TO ADP-RBOSYLATE EUKARYOTC RNA BINDING PROTENS

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    The bacterial plant pathogen Pseudomonas Syringae injects effector proteins into host cells via a type III protein secre tion system to cause disease. The invention relates to the discovery that the type III effector HopU1 is a mono-ADP ribosyltransferase (ADP-RT) and suppresses plant innate immunity. The HopU1 substrates in Arabidopsis thaliana extracts were RNA-binding proteins that possess RNA recognition motifs (RRMs). A. thaliana knock-out lines defective in the glycine-rich RNA-binding protein AtGRP7, a HopU1 substrate, were more susceptible than wild type plants to P syringae. The ADP-ribosylation of AtGRP7 by HopU1 required two arginines within the RRM. The inven tion provides novel methods for the modulation of the innate immune response of a plant to a biotic stress, including methods for enhancing or suppressing the innate immune response of the plant

    Phytopathogen type III effector weaponry and their plant targets

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    Phytopathogenic bacteria suppress plant innate immunity and promote pathogenesis by injecting proteins called type III effectors into plant cells using a type III protein secretion system. These type III effectors use at least three major strategies to alter host responses. One strategy is to alter host protein turnover, either by direct cleavage or by modulating ubiquitination and targeting to the 26S proteasome. Another strategy involves alteration of RNA metabolism by transcriptional activation or ADP-ribosylation of RNA-binding proteins. A third major strategy is to inhibit the kinases involved in plant defence signalling, either by removing phosphates or by direct inhibition. The wide array of strategies bacterial pathogens employ to suppress innate immunity suggest that circumvention of innate immunity is critical for bacterial pathogenicity of plants

    Phytopathogen type III effector weaponry and their plant targets

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    Phytopathogenic bacteria suppress plant innate immunity and promote pathogenesis by injecting proteins called type III effectors into plant cells using a type III protein secretion system. These type III effectors use at least three major strategies to alter host responses. One strategy is to alter host protein turnover, either by direct cleavage or by modulating ubiquitination and targeting to the 26S proteasome. Another strategy involves alteration of RNA metabolism by transcriptional activation or ADP-ribosylation of RNA-binding proteins. A third major strategy is to inhibit the kinases involved in plant defence signalling, either by removing phosphates or by direct inhibition. The wide array of strategies bacterial pathogens employ to suppress innate immunity suggest that circumvention of innate immunity is critical for bacterial pathogenicity of plants

    In vitro corrosion behavior and cytocompatibility of pure Fe implanted with Ta

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    In this study, pure Fe was surface-modified by Ta ion implantation with different incident ion doses. Its surface morphology and chemical composition were investigated using atomic force microscopy and auger electron spectroscopy. Results showed that Ta ion implantation led to the formation of Ta/Fe oxide mixtures at the outmost surface (60–80 nm in thickness) of the implanted layer. Results from electrochemical measurements and immersion tests indicated that the corrosion rate of the pure Fe in simulated body fluids can be accelerated after the Ta ion implantation. The in vitro cell culture results showed that the cytocompatibility of osteoblasts on the pure Fe has been significantly improved by applying the Ta ion implantation

    Damage Effects of Fluid filled Submunitions by High Velocity Projectile Impact

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    A series of tests investigating the damage effects of fluid-filled submunitions by high velocity projectile impact were conducted. An analytical model is presented, in which the yaw angle of the projectile was taken into account. Based on the analytical model, the influence of the strike angle, hit-point offset distance and projectile length to diameter ratio on submunition damage ratio were predicted. The analytical results showed a good agreement with the experiments. The submunition damage ratio strongly depends on the hit-point offset distance, showing a significant decrease with increasing hit-point offset distance. For large hit-point offset distance, increasing the length to diameter ratio of the projectile will effectively improve the submunition damage ratio. There is an appropriate yaw angle of the projectile in which the submunition damage ratio will be maximal

    The Pseudomonas syringae type III-secreted protein HopPtoD2 possesses protein tyrosine phosphatase activity and suppresses programmed cell death in plants

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    The bacterial plant pathogen Pseudomonas syringae possesses a type III protein secretion system that delivers many virulence proteins into plant cells. A subset of these proteins (called Avr proteins) is recognized by the plant’s innate immune system and triggers defences. One defence-associated response is the hypersensitive response (HR), a programmed cell death (PCD) of plant tissue. We have previously identified HopPtoD2 as a type III secreted protein from P. s. pv. tomato DC3000. Sequence analysis revealed that an N-terminal domain shared homology with Avr- PphD and a C-terminal domain was similar to protein tyrosine phosphatases (PTPs). We demonstrated that purified HopPtoD2 possessed PTP activity and this activity required a conserved catalytic Cys residue (Cys 378 ). Interestingly, HopPtoD2 was capable of suppressing the HR elicited by an avirulent P. syringae strain on Nicotiana benthamiana . HopPtoD2 derivatives that lacked Cys 378 no longer suppressed the HR indicating that HR suppression required PTP activity. A constitutively active MAPK kinase, called NtMEK2 DD , is capable of eliciting an HR-like cell death when transiently expressed in tobacco. When NtMEK2 DD and HopPtoD2 were co-delivered into plant cells, the HR was suppressed indicating that HopPtoD2 acts downstream of NtMEK2 DD . DC3000 hopPtoD2 mutants were slightly reduced in their ability to multiply in planta and displayed an enhanced ability to elicit an HR. The identification of HopPtoD2 as a PTP and a PCD suppressor suggests that the inactivation of MAPK pathways is a virulence strategy utilized by bacterial plant pathogens
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