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      Antibodies to the period gene product of drosophila reveal diverse tissue distribution and rhythmic changes in the visual system

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      Neuron
      Elsevier BV

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          Abstract

          Polyclonal antibodies were prepared against the period gene product, which influences biological rhythms in D. melanogaster, by using small synthetic peptides from the per sequence as immunogens. The peptide that elicited the best antibody reagent was a small domain near the site of the pers (short period) mutation. Specific immunohistochemical staining was detected in a variety of tissue types: the embryonic CNS; a few cell bodies in the central brain of pupae; these and other cells in the central brain of adults, as well as imaginal cells in the eyes, optic lobes, and the gut. The intensity of per-specific staining in the visual system was found to oscillate, defining a free-running circadian rhythm with a peak in the middle of the night.

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          Rod outer segment disk shedding in rat retina: relationship to cyclic lighting.

          When albino rats are reared in cyclic light, a burst of rod outer segment disk shedding occurs in the retina soon after the onset of light. The number of large packets of outer segment disks (phagosomes) in the pigment epithelium at this time is 2.5 to 5 times greater than at any other time of day or night. The subsequent degradation of large phagosomes to smaller structures within pigment epithelial cells proceeds rapidly. The burst of disk shedding follows a circadian rhythm for at least 3 days, since it occurs in continuous darkness at the same time without the onset of light.
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            Molecular analysis of the period locus in Drosophila melanogaster and identification of a transcript involved in biological rhythms.

            We have isolated and analyzed DNA sequences encompassing the period (per) locus of Drosophila melanogaster. The location of this clock gene was delimited by the molecular mapping of chromosome aberrations at or very near the per locus. At least five RNAs are transcribed from this region. One of these transcripts, a 0.9 kb species, is strongly implicated in per's control of biological rhythms. Two independently isolated arrhythmic mutations at the per locus dramatically reduce the level of this transcript. Furthermore, the level of the 0.9 kb transcript is strongly modulated during a light/dark cycle. We discuss evidence, from previously reported genetic and phenotypic analysis of per's function, suggesting that this region may be complex and that several gene products from the per region, including this 0.9 kb transcript, may be involved in the different aspects of normal rhythmicity influenced by this clock gene.
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              Characterization and cloning of fasciclin III: a glycoprotein expressed on a subset of neurons and axon pathways in Drosophila.

              To identify candidates for neuronal recognition molecules in Drosophila, we used monoclonal antibodies to search for surface glycoproteins expressed on subsets of axon bundles (or fascicles) during development. Here we report on the characterization and cloning of fasciclin III, which is expressed on a subset of neurons and axon pathways in the Drosophila embryo. Fasciclin III is also expressed at other times and places including transient segmentally repeated patches in the neuroepithelium and segmentally repeated stripes in the body epidermis. Antisera generated against each of four highly related forms of the protein were used for cDNA expression cloning to identify a single gene, which was confirmed to encode fasciclin III by tissue in situ hybridization and genetic deficiency analysis.
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                Author and article information

                Journal
                Neuron
                Neuron
                Elsevier BV
                08966273
                April 1988
                April 1988
                : 1
                : 2
                : 141-150
                Article
                10.1016/0896-6273(88)90198-5
                3152288
                e82ff023-ed9a-4ac3-8b18-2054ecf5b0c7
                © 1988

                https://www.elsevier.com/tdm/userlicense/1.0/

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