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      Immune pathways and defence mechanisms in honey bees Apis mellifera

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          Abstract

          Social insects are able to mount both group-level and individual defences against pathogens. Here we focus on individual defences, by presenting a genome-wide analysis of immunity in a social insect, the honey bee Apis mellifera. We present honey bee models for each of four signalling pathways associated with immunity, identifying plausible orthologues for nearly all predicted pathway members. When compared to the sequenced Drosophila and Anopheles genomes, honey bees possess roughly one-third as many genes in 17 gene families implicated in insect immunity. We suggest that an implied reduction in immune flexibility in bees reflects either the strength of social barriers to disease, or a tendency for bees to be attacked by a limited set of highly coevolved pathogens.

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          Most cited references 89

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          Multiple sequence alignment with the Clustal series of programs.

           R Chenna (2003)
          The Clustal series of programs are widely used in molecular biology for the multiple alignment of both nucleic acid and protein sequences and for preparing phylogenetic trees. The popularity of the programs depends on a number of factors, including not only the accuracy of the results, but also the robustness, portability and user-friendliness of the programs. New features include NEXUS and FASTA format output, printing range numbers and faster tree calculation. Although, Clustal was originally developed to run on a local computer, numerous Web servers have been set up, notably at the EBI (European Bioinformatics Institute) (http://www.ebi.ac.uk/clustalw/).
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            The dorsoventral regulatory gene cassette spätzle/Toll/cactus controls the potent antifungal response in Drosophila adults.

            The cytokine-induced activation cascade of NF-kappaB in mammals and the activation of the morphogen dorsal in Drosophila embryos show striking structural and functional similarities (Toll/IL-1, Cactus/I-kappaB, and dorsal/NF-kappaB). Here we demonstrate that these parallels extend to the immune response of Drosophila. In particular, the intracellular components of the dorsoventral signaling pathway (except for dorsal) and the extracellular Toll ligand, spätzle, control expression of the antifungal peptide gene drosomycin in adults. We also show that mutations in the Toll signaling pathway dramatically reduce survival after fungal infection. Antibacterial genes are induced either by a distinct pathway involving the immune deficiency gene (imd) or by combined activation of both imd and dorsoventral pathways.
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              Evolutionary ecology of insect immune defenses.

              Evolutionary ecology seeks to understand the selective reasons for the design features of the immune defense, especially with respect to parasitism. The molecular processes thereby set limitations, such as the failure to recognize an antigen, response specificity, the cost of defense, and the risk of autoimmunity. Sex, resource availability, and interference by parasites also affect a response. In turn, the defense repertoire consists of different kinds of immune responses--constitutive or induced, general or specific--and involves memory and lasting protection. Because the situation often defies intuition, mathematical analysis is typically required to identify the costs and benefits of variation in design, but such studies are few. In all, insect immune defense is much more similar to that of vertebrates than previously thought. In addition, the field is now rapidly becoming revolutionized by molecular data and methods that allow unprecedented access to study evolution in action.
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                Author and article information

                Journal
                Insect Mol Biol
                imb
                Insect Molecular Biology
                Blackwell Publishing Ltd
                0962-1075
                1365-2583
                01 October 2006
                : 15
                : 5
                : 645-656
                Affiliations
                [* ]USDA-ARS Bee Research Laboratory Beltsville, MD, USA
                []USDA-ARS Beneficial Insects Laboratory Weslaco, TX, USA
                []Institut de Biologie Moléculaire et Cellulaire CNRS, Strasbourg, France
                [§ ]Dept. Entomology, Oklahoma State University USA
                []Dept. Biochemistry, Kansas State University USA
                [** ]School of Biological Sciences, University of Sydney NSW, Australia
                [†† ]Umea Centre for Molecular Pathogenesis, Umea University Sweden
                Author notes
                Correspondence: J. D. Evans, USDA-ARS Bee Research Laboratory BARC-E Bldg 476 Beltsville, MD 20705, USA. Tel.: +1 301 504 5143; fax: +1 301 504 8736; e-mail: evansj@ 123456ba.ars.usda.gov .

                Re-use of this article is permitted in accordance with the Creative Commons Deed, Attribution 2·5, which does not permit commercial exploitation.

                Article
                10.1111/j.1365-2583.2006.00682.x
                1847501
                17069638
                © 2006 The Authors Journal compilation © 2006 The Royal Entomological Society
                Categories
                Special Issue: The Honey Bee Genome

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