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      Drosophila PQBP1 Regulates Learning Acquisition at Projection Neurons in Aversive Olfactory Conditioning

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          Abstract

          Polyglutamine tract-binding protein-1 (PQBP1) is involved in the transcription-splicing coupling, and its mutations cause a group of human mental retardation syndromes. We generated a fly model in which the Drosophila homolog of PQBP1 (dPQBP1) is repressed by insertion of piggyBac. In classical odor conditioning, learning acquisition was significantly impaired in homozygous piggyBac-inserted flies, whereas the following memory retention was completely normal. Mushroom bodies (MBs) and antennal lobes were morphologically normal in dPQBP1-mutant flies. Projection neurons (PNs) were not reduced in number and their fiber connections were not changed, whereas gene expressions including NMDA receptor subunit 1 (NR1) were decreased in PNs. Targeted double-stranded RNA-mediated silencing of dPQBP1 in PNs, but not in MBs, similarly disrupted learning acquisition. NR1 overexpression in PNs rescued the learning disturbance of dPQBP1 mutants. HDAC (histone deacetylase) inhibitors, SAHA (suberoylanilide hydroxamic acid) and PBA (phenylbutyrate), that upregulated NR1 partially rescued the learning disturbance. Collectively, these findings identify dPQBP1 as a novel gene regulating learning acquisition at PNs.

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          Author and article information

          Journal
          J Neurosci
          J. Neurosci
          jneuro
          jneurosci
          J. Neurosci
          The Journal of Neuroscience
          Society for Neuroscience
          0270-6474
          1529-2401
          20 October 2010
          : 30
          : 42
          : 14091-14101
          Affiliations
          [1] 1Department of Neuropathology, Medical Research Institute, Tokyo Medical and Dental University, Tokyo 113-8510, Japan,
          [2] 2Institute of Biotechnology, National Tsing Hua University, Hsinchu 30013, Taiwan, Republic of China,
          [3] 3Department of Biomolecular Science, Faculty of Science, Toho University, Chiba 274-8510, Japan,
          [4] 4Tokyo Metropolitan Institute for Neuroscience, Tokyo 183-8526, Japan,
          [5] 5Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, and
          [6] 6Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Kawaguchi 332-0012, Japan
          Author notes
          Correspondence should be addressed to Hitoshi Okazawa, Department of Neuropathology, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, Tokyo 113-8510, Japan. okazawa-tky@ 123456umin.ac.jp
          Article
          PMC6634781 PMC6634781 6634781 3640316
          10.1523/JNEUROSCI.1319-10.2010
          6634781
          20962230
          0f6f19df-5e3c-44dc-9d68-b4d60be92205
          Copyright © 2010 the authors 0270-6474/10/3014091-11$15.00/0
          History
          : 15 March 2010
          : 15 August 2010
          : 18 August 2010
          Categories
          Articles
          Neurobiology of Disease

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