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000138900 0247_ $$2doi$$a10.1074/jbc.M116.757823
000138900 0247_ $$2pmid$$apmid:27702999
000138900 0247_ $$2pmc$$apmc:PMC5122779
000138900 0247_ $$2ISSN$$a0021-9258
000138900 0247_ $$2ISSN$$a1067-8816
000138900 0247_ $$2ISSN$$a1083-351X
000138900 0247_ $$2altmetric$$aaltmetric:12468371
000138900 037__ $$aDZNE-2020-05222
000138900 041__ $$aEnglish
000138900 082__ $$a540
000138900 1001_ $$0P:(DE-HGF)0$$aWakabayashi, Satoru$$b0
000138900 245__ $$aOhgata, the Single Drosophila Ortholog of Human Cereblon, Regulates Insulin Signaling-dependent Organismic Growth.
000138900 260__ $$aBethesda, Md.$$bSoc.60645$$c2016
000138900 264_1 $$2Crossref$$3online$$bAmerican Society for Biochemistry & Molecular Biology (ASBMB)$$c2016-10-04
000138900 264_1 $$2Crossref$$3print$$bAmerican Society for Biochemistry & Molecular Biology (ASBMB)$$c2016-11-25
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000138900 520__ $$aCereblon (CRBN) is a substrate receptor of the E3 ubiquitin ligase complex that is highly conserved in animals and plants. CRBN proteins have been implicated in various biological processes such as development, metabolism, learning, and memory formation, and their impairment has been linked to autosomal recessive non-syndromic intellectual disability and cancer. Furthermore, human CRBN was identified as the primary target of thalidomide teratogenicity. Data on functional analysis of CRBN family members in vivo, however, are still scarce. Here we identify Ohgata (OHGT), the Drosophila ortholog of CRBN, as a regulator of insulin signaling-mediated growth. Using ohgt mutants that we generated by targeted mutagenesis, we show that its loss results in increased body weight and organ size without changes of the body proportions. We demonstrate that ohgt knockdown in the fat body, an organ analogous to mammalian liver and adipose tissue, phenocopies the growth phenotypes. We further show that overgrowth is due to an elevation of insulin signaling in ohgt mutants and to the down-regulation of inhibitory cofactors of circulating Drosophila insulin-like peptides (DILPs), named acid-labile subunit and imaginal morphogenesis protein-late 2. The two inhibitory proteins were previously shown to be components of a heterotrimeric complex with growth-promoting DILP2 and DILP5. Our study reveals OHGT as a novel regulator of insulin-dependent organismic growth in Drosophila.
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000138900 650_7 $$2NLM Chemicals$$aCRBN protein, human
000138900 650_7 $$2NLM Chemicals$$aDrosophila Proteins
000138900 650_7 $$2NLM Chemicals$$aIlp5 protein, Drosophila
000138900 650_7 $$2NLM Chemicals$$aInsulins
000138900 650_7 $$0EC 3.4.-$$2NLM Chemicals$$aPeptide Hydrolases
000138900 650_2 $$2MeSH$$aAdaptor Proteins, Signal Transducing
000138900 650_2 $$2MeSH$$aAnimals
000138900 650_2 $$2MeSH$$aCell Line
000138900 650_2 $$2MeSH$$aDrosophila Proteins: genetics
000138900 650_2 $$2MeSH$$aDrosophila Proteins: metabolism
000138900 650_2 $$2MeSH$$aDrosophila melanogaster
000138900 650_2 $$2MeSH$$aGene Knockdown Techniques
000138900 650_2 $$2MeSH$$aHumans
000138900 650_2 $$2MeSH$$aInsulins: genetics
000138900 650_2 $$2MeSH$$aInsulins: metabolism
000138900 650_2 $$2MeSH$$aPeptide Hydrolases: genetics
000138900 650_2 $$2MeSH$$aPeptide Hydrolases: metabolism
000138900 650_2 $$2MeSH$$aSignal Transduction: physiology
000138900 650_2 $$2MeSH$$aUbiquitin-Protein Ligases
000138900 7001_ $$0P:(DE-HGF)0$$aSawamura, Naoya$$b1$$eCorresponding author
000138900 7001_ $$0P:(DE-HGF)0$$aVoelzmann, André$$b2
000138900 7001_ $$0P:(DE-2719)2810307$$aBrömer, Meike$$b3$$udzne
000138900 7001_ $$0P:(DE-HGF)0$$aAsahi, Toru$$b4
000138900 7001_ $$0P:(DE-HGF)0$$aHoch, Michael$$b5
000138900 77318 $$2Crossref$$3journal-article$$a10.1074/jbc.m116.757823$$b : American Society for Biochemistry & Molecular Biology (ASBMB), 2016-10-04$$n48$$p25120-25132$$tJournal of Biological Chemistry$$v291$$x0021-9258$$y2016
000138900 773__ $$0PERI:(DE-600)1474604-9$$a10.1074/jbc.M116.757823$$gVol. 291, no. 48, p. 25120 - 25132$$n48$$p25120-25132$$q291:48<25120 - 25132$$tThe journal of biological chemistry$$v291$$x0021-9258$$y2016
000138900 8567_ $$2Pubmed Central$$uhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC5122779
000138900 909CO $$ooai:pub.dzne.de:138900$$pVDB
000138900 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2810307$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b3$$kDZNE
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000138900 9141_ $$y2016
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000138900 915__ $$0StatID:(DE-HGF)0100$$2StatID$$aJCR$$bJ BIOL CHEM : 2017
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