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Cell Death Response (cell + death_response)
Selected AbstractsA mutation in the Arabidopsis mTERF-related plastid protein SOLDAT10 activates retrograde signaling and suppresses 1O2 -induced cell deathTHE PLANT JOURNAL, Issue 3 2009Rasa Meskauskiene Summary The conditional flu mutant of Arabidopsis thaliana generates singlet oxygen (1O2) in plastids during a dark-to-light shift. Seedlings of flu bleach and die, whereas mature plants stop growing and develop macroscopic necrotic lesions. Several suppressor mutants, dubbed singlet oxygen-linked death activator (soldat), were identified that abrogate 1O2 -mediated cell death of flu seedlings. One of the soldat mutations, soldat10, affects a gene encoding a plastid-localized protein related to the human mitochondrial transcription termination factor mTERF. As a consequence of this mutation, plastid-specific rRNA levels decrease and protein synthesis in plastids of soldat10 is attenuated. This disruption of chloroplast homeostasis in soldat10 seedlings affects communication between chloroplasts and the nucleus and leads to changes in the steady-state concentration of nuclear gene transcripts. The soldat10 seedlings suffer from mild photo-oxidative stress, as indicated by the constitutive up-regulation of stress-related genes. Even though soldat10/flu seedlings overaccumulate the photosensitizer protochlorophyllide in the dark and activate the expression of 1O2 -responsive genes after a dark-to-light shift they do not show a 1O2 -dependent cell death response. Disturbance of chloroplast homeostasis in emerging soldat10/flu seedlings seems to antagonize a subsequent 1O2 -mediated cell death response without suppressing 1O2 -dependent retrograde signaling. The results of this work reveal the unexpected complexity of what is commonly referred to as ,plastid signaling'. [source] SIPK signaling controls multiple components of harpin-induced cell death in tobaccoTHE PLANT JOURNAL, Issue 3 2005Marcus A. Samuel Summary Harpin from Pseudomonas syringae pv. phaseolicola (HrpZ) elicits a rapid cell death response in tobacco plants. Multiple signaling components, including mitogen-activated protein kinase (MAPK), reactive oxygen species (ROS) and salicylic acid (SA), have been reported to be involved in this cell death process, but the interaction between these molecules is poorly understood. Here we show through utilizing plants manipulated in SIPK expression levels that lack of SIPK results in increased sensitivity to harpin with concomitant accumulation of higher levels of ROS. Conversely, SIPK-overexpressing plants show reduced sensitivity to harpin relative to wild-type plants, and display reduced ROS accumulation. Harpin-induced cell death was found to be conditional on the ability of the plant to accumulate SA, whereas harpin induction of MAPK activation and ROS accumulation are not. However, harpin-induced ROS accumulation is required for activation of SIPK and wound-induced protein kinase. Transcriptional profiling revealed that suppression of SIPK signaling also affects early expression of a range of pathogen- and stress-responsive genes during harpin challenge. [source] The conserved Xanthomonas campestris pv. vesicatoria effector protein XopX is a virulence factor and suppresses host defense in Nicotiana benthamianaTHE PLANT JOURNAL, Issue 6 2005Matthew Metz Summary Nicotiana benthamiana leaves display a visible plant cell death response when infiltrated with a high titer inoculum of the non-host pathogen, Xanthomonas campestris pv. vesicatoria (Xcv). This visual phenotype was used to identify overlapping cosmid clones from a genomic cosmid library constructed from the Xcv strain, GM98-38. Individual cosmid clones from the Xcv library were conjugated into X. campestris pv. campestris (Xcc) and exconjugants were scored for an altered visual high titer inoculation response in N. benthamiana. The molecular characterization of the cosmid clones revealed that they contained a novel gene, xopX, that encodes a 74-kDa type III secretion system (TTSS) effector protein. Agrobacterium -mediated transient expression of XopX in N. benthamiana did not elicit the plant cell death response although detectable XopX protein was produced. Interestingly, the plant cell death response occurred when the xopX Agrobacterium -mediated transient expression construct was co-inoculated with strains of either Xcv,xopX or Xcc, both lacking xopX. The co-inoculation complementation of the plant cell death response also depends on whether the Xanthomonas strains contain an active TTSS. Transgenic 35S- xopX -expressing N. benthamiana plants also have the visible plant cell death response when inoculated with the non- xopX -expressing strains Xcv,xopX and Xcc. Unexpectedly, transgenic 35S- xopX N. benthamiana plants displayed enhanced susceptibility to bacterial growth of Xcc as well as other non- xopX -expressing Xanthomonas and Pseudomonas strains. This result is also consistent with the increase in bacterial growth on wild type N. benthamiana plants observed for Xcc when XopX is expressed in trans. Furthermore, XopX contributes to the virulence of Xcv on host pepper (Capsicum annuum) and tomato (Lycopersicum esculentum) plants. We propose that the XopX bacterial effector protein targets basic innate immunity in plants, resulting in enhanced plant disease susceptibility. [source] Sclerotinia sclerotiorum: When "to be or not to be" a pathogen?FEMS MICROBIOLOGY LETTERS, Issue 2 2005Dwayne D. Hegedus Abstract Sclerotinia sclerotiorum is unusual among necrotrophic pathogens in its requirement for senescent tissues to establish an infection and to complete the life cycle. A model for the infection process has emerged whereby the pathogenic phase is bounded by saprophytic phases; the distinction being that the dead tissues in the latter are generated by the actions of the pathogen. Initial colonization of dead tissue provides nutrients for pathogen establishment and resources to infect healthy plant tissue. The early pathogenicity stage involves production of oxalic acid and the expression of cell wall degrading enzymes, such as specific isoforms of polygalacturonase (SSPG1) and protease (ASPS), at the expanding edge of the lesion. Such activities release small molecules (oligo-galacturonides and peptides) that serve to induce the expression of a second wave of degradative enzymes that collectively bring about the total dissolution of the plant tissue. Oxalic acid and other metabolites and enzymes suppress host defences during the pathogenic phase, while other components initiate host cell death responses leading to the formation of necrotic tissue. The pathogenic phase is followed by a second saprophytic phase, the transition to which is effected by declining cAMP levels as glucose becomes available and further hydrolytic enzyme synthesis is repressed. Low cAMP levels and an acidic environment generated by the secretion of oxalic acid promote sclerotial development and completion of the life cycle. This review brings together histological, biochemical and molecular information gathered over the past several decades to develop this tri-phasic model for infection. In several instances, studies with Botrytis species are drawn upon for supplemental and supportive evidence for this model. In this process, we attempt to outline how the interplay between glucose levels, cAMP and ambient pH serves to coordinate the transition between these phases and dictate the biochemical and developmental events that define them. [source] Pyroptosis and host cell death responses during Salmonella infectionCELLULAR MICROBIOLOGY, Issue 11 2007Susan L. Fink Summary Salmonella enterica are facultatively intracellular pathogens causing diseases with markedly visible signs of inflammation. During infection, Salmonella interacts with various host cell types, often resulting in death of those cells. Salmonella induces intestinal epithelial cell death via apoptosis, a cell death programme with a notably non-inflammatory outcome. In contrast, macrophage infection triggers caspase-1-dependent proinflammatory programmed cell death, a recently recognized process termed pyroptosis, which is distinguished from other forms of cellular demise by its unique mechanism, features and inflammatory outcome. Rapid macrophage pyroptosis depends on the Salmonella pathogenicity island-1 type III secretion system (T3SS) and flagella. Salmonella dynamically modulates induction of macrophage pyroptosis, and regulation of T3SS systems permits bacterial replication in specialized intracellular niches within macrophages. However, these infected macrophages later undergo a delayed form of caspase-1-dependent pyroptosis. Caspase-1-deficient mice are more susceptible to a number of bacterial infections, including salmonellosis, and pyroptosis is therefore considered a generalized protective host response to infection. Thus, Salmonella -induced pyroptosis serves as a model to understand a broadly important pathway of proinflammatory programmed host cell death: examining this system affords insight into mechanisms of both beneficial and pathological cell death and strategies employed by pathogens to modulate host responses. [source] | ||||||||||