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      Identification of genes differentially expressed during interaction of resistant and susceptible apple cultivars ( Malus × domestica) with Erwinia amylovora

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          Abstract

          Background

          The necrogenic enterobacterium, Erwinia amylovora is the causal agent of the fire blight (FB) disease in many Rosaceaespecies, including apple and pear. During the infection process, the bacteria induce an oxidative stress response with kinetics similar to those induced in an incompatible bacteria-plant interaction. No resistance mechanism to E. amylovora in host plants has yet been characterized, recent work has identified some molecular events which occur in resistant and/or susceptible host interaction with E. amylovora: In order to understand the mechanisms that characterize responses to FB, differentially expressed genes were identified by cDNA-AFLP analysis in resistant and susceptible apple genotypes after inoculation with E. amylovora.

          Results

          cDNA were isolated from M.26 (susceptible) and G.41 (resistant) apple tissues collected 2 h and 48 h after challenge with a virulent E. amylovora strain or mock (buffer) inoculated. To identify differentially expressed transcripts, electrophoretic banding patterns were obtained from cDNAs. In the AFLP experiments, M.26 and G.41 showed different patterns of expression, including genes specifically induced, not induced, or repressed by E. amylovora. In total, 190 ESTs differentially expressed between M.26 and G.41 were identified using 42 pairs of AFLP primers. cDNA-AFLP analysis of global EST expression in a resistant and a susceptible apple genotype identified different major classes of genes. EST sequencing data showed that genes linked to resistance, encoding proteins involved in recognition, signaling, defense and apoptosis, were modulated by E. amylovora in its host plant. The expression time course of some of these ESTs selected via a bioinformatic analysis has been characterized.

          Conclusion

          These data are being used to develop hypotheses of resistance or susceptibility mechanisms in Malus to E. amylovora and provide an initial categorization of genes possibly involved in recognition events, early signaling responses the subsequent development of resistance or susceptibility. These data also provided potential candidates for improving apple resistance to fire blight either by marker-assisted selection or genetic engineering.

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          Most cited references30

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          THE OXIDATIVE BURST IN PLANT DISEASE RESISTANCE.

          Rapid generation of superoxide and accumulation of H2O2 is a characteristic early feature of the hypersensitive response following perception of pathogen avirulence signals. Emerging data indicate that the oxidative burst reflects activation of a membrane-bound NADPH oxidase closely resembling that operating in activated neutrophils. The oxidants are not only direct protective agents, but H2O2 also functions as a substrate for oxidative cross-linking in the cell wall, as a threshold trigger for hypersensitive cell death, and as a diffusible signal for induction of cellular protectant genes in surrounding cells. Activation of the oxidative burst is a central component of a highly amplified and integrated signal system, also involving salicylic acid and perturbations of cytosolic Ca2+, which underlies the expression of disease-resistance mechanisms.
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            Type III secretion machines: bacterial devices for protein delivery into host cells.

            Several Gram-negative pathogenic bacteria have evolved a complex protein secretion system termed type III to deliver bacterial effector proteins into host cells that then modulate host cellular functions. These bacterial devices are present in both plant and animal pathogenic bacteria and are evolutionarily related to the flagellar apparatus. Although type III secretion systems are substantially conserved, the effector molecules they deliver are unique for each bacterial species. Understanding the biology of these devices may allow the development of novel prevention and therapeutic approaches for several infectious diseases.
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              Death Don't Have No Mercy: Cell Death Programs in Plant-Microbe Interactions.

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                Author and article information

                Journal
                BMC Plant Biol
                BMC Plant Biology
                BioMed Central
                1471-2229
                2010
                4 January 2010
                : 10
                : 1
                Affiliations
                [1 ]FEM-IASMA Research Centre, Via E. Mach 1, 38010 San Michele all'Adige (TN) Italy
                [2 ]Department of Plant Pathology, Cornell University, 630 W. North St., Geneva, NY 14456 USA
                [3 ]USDA-ARS Plant Genetic Resources Unit, 630 W. North St., Geneva, NY 14456 USA
                [4 ]USDA-ARS Appalachian Fruit Research Station, 2217 Wiltshire Rd, Kearneysville, WV, 25430
                [5 ]Pennsylvania State University, 1031 Edgecomb Avenue, York, PA, 17403 USA
                Article
                1471-2229-10-1
                10.1186/1471-2229-10-1
                2827420
                20047654
                b6abd4ba-1d2a-41fd-b687-0144403ac987
                Copyright ©2010 Baldo et al; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 8 June 2009
                : 4 January 2010
                Categories
                Research article

                Plant science & Botany
                Plant science & Botany

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