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      Feedback from Rhodopsin controls rhodopsin exclusion in Drosophila photoreceptors

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          Abstract

          Sensory systems with high discriminatory power employ neurons that express only one of several alternative sensory receptor proteins. This exclusive receptor gene expression restricts the sensitivity spectrum of neurons and is coordinated with the choice of their synaptic targets 1- 3 . However, little is known about how it is maintained throughout the life of a neuron. Here we show that the green-light sensing receptor Rhodopsin 6 (Rh6) acts to exclude an alternative blue-sensitive Rhodopsin 5 (Rh5) from a subset of Drosophila R8 photoreceptor neurons 4 . Loss of Rh6 leads to a gradual expansion of Rh5 expression into all R8 photoreceptors of the aging adult retina. The Rh6 feedback signal results in repression of the rh5 promoter and can be mimicked by other Drosophila Rhodopsins; it is partially dependent on activation of Rhodopsin by light, and relies on G αq activity, but not on the subsequent steps of the phototransduction cascade 5 . Our observations reveal a thus far unappreciated spectral plasticity of R8 photoreceptors, and identify Rhodopsin feedback as an exclusion mechanism.

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          Most cited references42

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          An optimized transgenesis system for Drosophila using germ-line-specific phiC31 integrases.

          Germ-line transformation via transposable elements is a powerful tool to study gene function in Drosophila melanogaster. However, some inherent characteristics of transposon-mediated transgenesis limit its use for transgene analysis. Here, we circumvent these limitations by optimizing a phiC31-based integration system. We generated a collection of lines with precisely mapped attP sites that allow the insertion of transgenes into many different predetermined intergenic locations throughout the fly genome. By using regulatory elements of the nanos and vasa genes, we established endogenous sources of the phiC31 integrase, eliminating the difficulties of coinjecting integrase mRNA and raising the transformation efficiency. Moreover, to discriminate between specific and rare nonspecific integration events, a white gene-based reconstitution system was generated that enables visual selection for precise attP targeting. Finally, we demonstrate that our chromosomal attP sites can be modified in situ, extending their scope while retaining their properties as landing sites. The efficiency, ease-of-use, and versatility obtained here with the phiC31-based integration system represents an important advance in transgenesis and opens up the possibility of systematic, high-throughput screening of large cDNA sets and regulatory elements.
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            Exploiting position effects and the gypsy retrovirus insulator to engineer precisely expressed transgenes.

            A major obstacle to creating precisely expressed transgenes lies in the epigenetic effects of the host chromatin that surrounds them. Here we present a strategy to overcome this problem, employing a Gal4-inducible luciferase assay to systematically quantify position effects of host chromatin and the ability of insulators to counteract these effects at phiC31 integration loci randomly distributed throughout the Drosophila genome. We identify loci that can be exploited to deliver precise doses of transgene expression to specific tissues. Moreover, we uncover a previously unrecognized property of the gypsy retrovirus insulator to boost gene expression to levels severalfold greater than at most or possibly all un-insulated loci, in every tissue tested. These findings provide the first opportunity to create a battery of transgenes that can be reliably expressed at high levels in virtually any tissue by integration at a single locus, and conversely, to engineer a controlled phenotypic allelic series by exploiting several loci. The generality of our approach makes it adaptable to other model systems to identify and modify loci for optimal transgene expression.
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              Identifying tumor suppressors in genetic mosaics: the Drosophila lats gene encodes a putative protein kinase.

              We have identified recessive overproliferation mutations by screening and examining clones of mutant cells in genetic mosaics of the fruitfly Drosophila melanogaster. This type of screen provides a powerful approach for identifying and studying potential tumor suppressors. One of the identified genes, lats, has been cloned and encodes a putative protein kinase that shares high levels of sequence similarity with three proteins in budding yeast and Neurospora that are involved in regulation of the cell cycle and growth. Mutations in lats cause dramatic overproliferation phenotypes and various developmental defects in both mosaic animals and homozygous mutants.
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                Author and article information

                Journal
                0410462
                6011
                Nature
                Nature
                Nature
                0028-0836
                1476-4687
                17 August 2011
                9 October 2011
                3 May 2012
                : 479
                : 7371
                : 108-112
                Affiliations
                [1 ]Center for Developmental Genetics, Department of Biology, New York University, New York NY 10003
                Author notes
                [2]

                present address: Departments of Pathology, Neurology, and Neuroscience, Columbia University Medical Center, 630 W 168 Street, New York, NY 10032

                [3]

                present address: Department of Biology, University of Fribourg, Chemin du Musée 10, 1700 Fribourg, Switzerland

                [4]

                present address: Department of Molecular Biology and Genetics, Bogazici University, 34342 Bebek, Istanbul, Turkey

                [(&) ]Correspondence and requests for materials should be addressed to ( cd38@ 123456nyu.edu ).
                Article
                nihpa318664
                10.1038/nature10451
                3208777
                21983964
                9214aacf-7f89-4ce1-b2ed-6ed8062fda45

                Users may view, print, copy, download and text and data- mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms

                History
                Funding
                Funded by: National Eye Institute : NEI
                Award ID: R01 EY013012-13 || EY
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