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      Behavioral genomics of honeybee foraging and nest defense

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          Abstract

          The honeybee has been the most important insect species for study of social behavior. The recently released draft genomic sequence for the bee will accelerate honeybee behavioral genetics. Although we lack sufficient tools to manipulate this genome easily, quantitative trait loci (QTLs) that influence natural variation in behavior have been identified and tested for their effects on correlated behavioral traits. We review what is known about the genetics and physiology of two behavioral traits in honeybees, foraging specialization (pollen versus nectar), and defensive behavior, and present evidence that map-based cloning of genes is more feasible in the bee than in other metazoans. We also present bioinformatic analyses of candidate genes within QTL confidence intervals (CIs). The high recombination rate of the bee made it possible to narrow the search to regions containing only 17–61 predicted peptides for each QTL, although CIs covered large genetic distances. Knowledge of correlated behavioral traits, comparative bioinformatics, and expression assays facilitated evaluation of candidate genes. An overrepresentation of genes involved in ovarian development and insulin-like signaling components within pollen foraging QTL regions suggests that an ancestral reproductive gene network was co-opted during the evolution of foraging specialization. The major QTL influencing defensive/aggressive behavior contains orthologs of genes involved in central nervous system activity and neurogenesis. Candidates at the other two defensive-behavior QTLs include modulators of sensory signaling ( Am5HT 7 serotonin receptor, AmArr4 arrestin, and GABA-B-R1 receptor). These studies are the first step in linking natural variation in honeybee social behavior to the identification of underlying genes.

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          Most cited references75

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          Mapping mendelian factors underlying quantitative traits using RFLP linkage maps.

          The advent of complete genetic linkage maps consisting of codominant DNA markers [typically restriction fragment length polymorphisms (RFLPs)] has stimulated interest in the systematic genetic dissection of discrete Mendelian factors underlying quantitative traits in experimental organisms. We describe here a set of analytical methods that modify and extend the classical theory for mapping such quantitative trait loci (QTLs). These include: (i) a method of identifying promising crosses for QTL mapping by exploiting a classical formula of SEWALL WRIGHT; (ii) a method (interval mapping) for exploiting the full power of RFLP linkage maps by adapting the approach of LOD score analysis used in human genetics, to obtain accurate estimates of the genetic location and phenotypic effect of QTLs; and (iii) a method (selective genotyping) that allows a substantial reduction in the number of progeny that need to be scored with the DNA markers. In addition to the exposition of the methods, explicit graphs are provided that allow experimental geneticists to estimate, in any particular case, the number of progeny required to map QTLs underlying a quantitative trait.
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            The genetics of addictions: uncovering the genes.

            The addictions are common chronic psychiatric diseases that today are prevented and treated using relatively untargeted and only partially effective methods. The addictions are moderately to highly heritable, which is paradoxical because these disorders require use; a choice that is itself modulated by both genes and environment. The addictions are interrelated and related to other psychiatric diseases by common neurobiological pathways, including those that modulate reward, behavioural control and the anxiety or stress response. Our future understanding of addictions will be enhanced by the identification of genes that have a role in altered substance-specific vulnerabilities such as variation in drug metabolism or drug receptors and a role in shared vulnerabilities such as variation in reward or stress resiliency.
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              Molecular structure and physiological functions of GABA(B) receptors.

              GABA(B) receptors are broadly expressed in the nervous system and have been implicated in a wide variety of neurological and psychiatric disorders. The cloning of the first GABA(B) receptor cDNAs in 1997 revived interest in these receptors and their potential as therapeutic targets. With the availability of molecular tools, rapid progress was made in our understanding of the GABA(B) system. This led to the surprising discovery that GABA(B) receptors need to assemble from distinct subunits to function and provided exciting new insights into the structure of G protein-coupled receptors (GPCRs) in general. As a consequence of this discovery, it is now widely accepted that GPCRs can exist as heterodimers. The cloning of GABA(B) receptors allowed some important questions in the field to be answered. It is now clear that molecular studies do not support the existence of pharmacologically distinct GABA(B) receptors, as predicted by work on native receptors. Advances were also made in clarifying the relationship between GABA(B) receptors and the receptors for gamma-hydroxybutyrate, an emerging drug of abuse. There are now the first indications linking GABA(B) receptor polymorphisms to epilepsy. Significantly, the cloning of GABA(B) receptors enabled identification of the first allosteric GABA(B) receptor compounds, which is expected to broaden the spectrum of therapeutic applications. Here we review current concepts on the molecular composition and function of GABA(B) receptors and discuss ongoing drug-discovery efforts.
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                Author and article information

                Contributors
                ghunt@purdue.edu
                nsardes@purdue.edu
                cwilliams@purdue.edu
                olav_rueppell@uncg.edu
                eguzman@uoguelph.ca
                are@servidor.unam.mx
                schandra@roosevelt.edu
                martin.beye@uni-dusseldorf.de
                repage@asu.edu
                Journal
                Naturwissenschaften
                Die Naturwissenschaften
                Springer-Verlag (Berlin/Heidelberg )
                0028-1042
                1432-1904
                15 December 2006
                April 2007
                : 94
                : 4
                : 247-267
                Affiliations
                [1 ]Department of Entomology, Purdue University, West Lafayette, IN 47907 USA
                [2 ]School of Life Sciences, Arizona State University, P.O. Box 87451, Tempe, AZ 85287-4501 USA
                [3 ]Department of Biological Sciences, Purdue University, West Lafayette, IN 47907 USA
                [4 ]Crop Production and Pest Control Research Unit, USDA-ARS, West Lafayette, IN 47906 USA
                [5 ]Department of Biology, University of North Carolina, 105 Eberhart Bldg., Greensboro, NC 27402 USA
                [6 ]Department of Environmental Biology, University of Guelph, N1G 2W1 Ontario, Canada
                [7 ]Centro Nacional de Investigación Disciplinaria en Fisiología Animal, INIFAP, Queretaro, Queretaro Mexico
                [8 ]Department of Biological, Chemical and Physical Sciences, Roosevelt University, Chicago, IL 60605 USA
                [9 ]Institut fuer Genetik, Heinrich-Heine Universitaet Duesseldorf, 40225 Duesseldorf, Germany
                Article
                183
                10.1007/s00114-006-0183-1
                1829419
                17171388
                1a0a1777-f436-4a48-a1cb-3187db8971b5
                © Springer-Verlag 2006
                History
                : 6 September 2006
                : 8 October 2006
                : 16 October 2006
                Categories
                Review
                Custom metadata
                © Springer-Verlag 2007

                Uncategorized
                behavior genetics,foraging behavior,apis mellifera,insulin-like signaling,aggressive behavior,candidate genes,recombination rate

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