Plant targets for \u3ci\u3ePseudomonas syringae\u3c/i\u3e type III effectors: Virulence targets or guarded decoys?

The phytopathogenic bacterium Pseudomonas syringae can suppress both pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) and effector-triggered immunity (ETI) by the injection of type III effector (T3E) proteins into host cells. T3Es achieve immune suppression using a variety of strategies including interference with immune receptor signaling, blocking RNA pathways and vesicle trafficking, and altering organelle function. T3Es can be recognized directly or indirectly by resistance proteins monitoring specific T3E targets resulting in ETI. It is presently unclear whether the monitored targets represent bona fide virulence targets or guarded decoys. Extensive overlap between PTI and ETI signaling suggests that T3Es may suppress both pathways through common targets and by possessing multiple activities

Plant Immunity Directly or Indirectly Restricts the Injection of Type III Effectors by the \u3ci\u3ePseudomonas syringae\u3c/i\u3e Type III Secretion System

Plants perceive microorganisms by recognizing microbial molecules known as pathogen-associated molecular patterns (PAMPs) inducing PAMP-triggered immunity (PTI) or by recognizing pathogen effectors inducing effector-triggered immunity (ETI). The hypersensitive response (HR), a programmed cell death response associated with ETI, is known to be inhibited by PTI. Here, we show that PTI-induced HR inhibition is due to direct or indirect restriction of the type III protein secretion system’s (T3SS) ability to inject type III effectors (T3Es). We found that the Pseudomonas syringae T3SS was restricted in its ability to inject a T3E-adenylate cyclase (CyaA) injection reporter into PTI-induced tobacco (Nicotiana tabacum) cells. We confirmed this restriction with a direct injection assay that monitored the in planta processing of the AvrRpt2 T3E. Virulent P. syringae strains were able to overcome a PAMP pretreatment in tobacco or Arabidopsis (Arabidopsis thaliana) and continue to inject a T3E-CyaA reporter into host cells. In contrast, ETI-inducing P. syringae strains were unable to overcome PTI-induced injection restriction. A P. syringae pv tomato DC3000 mutant lacking about one-third of its T3E inventory was less capable of injecting into PTI-induced Arabidopsis plant cells, grew poorly in planta, and did not cause disease symptoms. PTI-induced transgenic Arabidopsis expressing the T3E HopAO1 or HopF2 allowed higher amounts of the T3E-CyaA reporter to be injected into plant cells compared to wild-type plants. Our results show that PTI-induced HR inhibition is due to direct or indirect restriction of T3E injection and that T3Es can relieve this restriction by suppressing PTI

Phytopathogen type III effector weaponry and their plant targets

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

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

Matters of Life and Death

What is the significance of the concepts of ‘life’ and ‘death’ for different religious and non-religious groups? This chapter aims to draw out deeper understanding of practices of connection and separation between religious and non-religious groups through examining affinities between how different Christian and non-religious groups engage with notions of ‘life’ and ‘death’, drawing on qualitative sociological research. Although questions of life and death might appear perennial concerns for religion, I explore here the particular contemporary significance of ideas of ‘life’ and ‘death’ within the moral landscapes of different religious and non-religious groups. The chapter considers the significance of the idea of ‘life’ for an ‘open’ evangelical church, the Sunday Assembly, and the School of Life, and practices of reflecting on ‘death’ in Death Cafés, drawing this together with Georg Simmel’s writing on life and its interrelations with death. I conclude by suggesting that attending to modes of practical engagement with ideas of ‘life’ and ‘death’ across these different religious and non-religious groups, rather than focusing solely on the propositional content of beliefs about life and death, opens up opportunities for reflection on common existential grounds of experience, moving beyond assumptions that relations between these groups are necessarily antagonistic

'Bringing me more than I contain': Levinas, ethical subjectivity and the infinite demands of education

Emmanuel Levinas' s reorientation of ethics as preceding ontology and his radical\ud presentation of responsibility, justice, consciousness and knowledge are of clear\ud relevance for education. It is therefore not surprising that in the last decade we have\ud seen a number of studies ofLevinas by educational theorists.\ud Much of this work has focused on Levinas's relevance for issues of ethics, social\ud justice, multiculturalism and moral education. This thesis draws on this previous\ud research, but aims to take educational readings of Levinas in another direction\ud through considering how his presentation of discourse, language and subjectivity, as\ud dependent on an infinite ethical demand, troubles several dominant orientations\ud within educational discourse that treat education in ways that can become totalising\ud and instrumentalist.\ud I begin by offering a philosophical analysis of how Levinas describes the scene of\ud teaching and the nature of subjectivity. I then interrogate how this reading of Levinas\ud disturbs some current understandings of education: first, the way that, within\ud liberalism, education can be conceived instrumentally as the site for the development\ud of a certain kind of individual (a rationally autonomous chooser, etc.), and second, the\ud way that neoliberal educational ideologies have privileged managerialism,\ud performance and the market, with Religious Education providing a case study of the\ud implications of Levinas's interruption. I then consider how this leads to new\ud understandings of community and political subjectivity within education.\ud In this way, I explore how responding to Levinas, and reading his work together with\ud criticisms addressed by Badiou and others, leads us not just to a richer vision of the\ud meaning of education, but also to a more motivating understanding of the ethical\ud subjectivity of both students and teachers, which is dependent on a deepening and anarchic\ud responsibility, and which invites us to work for a better education extending\ud beyond the straight line ofthe law

Latour, Prepositions and the Instauration of Secularism

Bruno Latour's understanding of different modes of existence as given through prepositions offers a new approach to researching "secularism," taking forward attention paid in recent scholarship to its historically contingent formation by bringing into clearer focus the dynamics of its relational and material mediations. Examining the contemporary instauration of secularism in conservative evangelical experience, I show how this approach offers a new orientation to studying secularism that allows attention to both its history and its material effects on practice. This shows how Latour's speculative realism extends and provides a bridge between both discursive analysis of religion and secularism and the recent turn towards materiality in empirical study of religion

The \u3ci\u3ePseudomonas syringae \u3c/i\u3etype III effector HopG1 targets mitochondria, alters plant development, and suppresses plant innate immunity

The bacterial plant pathogen Pseudomonas syringae uses a type III protein secretion system to inject type III effectors into plant cells. Primary targets of these effectors appear to be effector-triggered immunity (ETI) and pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI). The type III effector HopG1 is a suppressor of ETI that is broadly conserved in bacterial plant pathogens. Here we show that HopG1 from P. syringae pv. tomato DC3000 also suppresses PTI. Interestingly, HopG1 localizes to plant mitochondria, suggesting that its suppression of innate immunity may be linked to a perturbation of mitochondrial function. While HopG1 possesses no obvious mitochondrial signal peptide, its N-terminal two-thirds was sufficient for mitochondrial localization. A HopG1-GFP fusion lacking HopG1’s N-terminal 13 amino acids was not localized to the mitochondria reflecting the importance of the N-terminus for targeting. Constitutive expression of HopG1 in Arabidopsis thaliana, Nicotiana tabacum (tobacco) and Lycopersicon esculentum (tomato) dramatically alters plant development resulting in dwarfism, increased branching and infertility. Constitutive expression of HopG1 in planta leads to reduced respiration rates and an increased basal level of reactive oxygen species. These findings suggest that HopG1’s target is mitochondrial and that effector/target interaction promotes disease by disrupting mitochondrial functions

The \u3ci\u3ePseudomonas syringae \u3c/i\u3etype III effector HopG1 targets mitochondria, alters plant development, and suppresses plant innate immunity

The bacterial plant pathogen Pseudomonas syringae uses a type III protein secretion system to inject type III effectors into plant cells. Primary targets of these effectors appear to be effector-triggered immunity (ETI) and pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI). The type III effector HopG1 is a suppressor of ETI that is broadly conserved in bacterial plant pathogens. Here we show that HopG1 from P. syringae pv. tomato DC3000 also suppresses PTI. Interestingly, HopG1 localizes to plant mitochondria, suggesting that its suppression of innate immunity may be linked to a perturbation of mitochondrial function. While HopG1 possesses no obvious mitochondrial signal peptide, its N-terminal two-thirds was sufficient for mitochondrial localization. A HopG1-GFP fusion lacking HopG1’s N-terminal 13 amino acids was not localized to the mitochondria reflecting the importance of the N-terminus for targeting. Constitutive expression of HopG1 in Arabidopsis thaliana, Nicotiana tabacum (tobacco) and Lycopersicon esculentum (tomato) dramatically alters plant development resulting in dwarfism, increased branching and infertility. Constitutive expression of HopG1 in planta leads to reduced respiration rates and an increased basal level of reactive oxygen species. These findings suggest that HopG1’s target is mitochondrial and that effector/target interaction promotes disease by disrupting mitochondrial functions