{"title":"分裂复合体增强子中的删除映射","authors":"Elisa Wurmbach, Anette Preiss","doi":"10.1111/hrd2.00065","DOIUrl":null,"url":null,"abstract":"<p>The <i>Enhancer of split complex [E(spl)-C]</i> comprises twelve genes of different classes. Seven genes encode proteins of with a basic-helix-loop-helix-orange (bHLH-O) domain that function as transcriptional repressors and serve as effectors of the Notch signalling pathway. They have been named <i>E(spl)m8-, m7-, m5-, m3-, mβ-, mγ-</i> and <i>mδ-HLH</i>. Four genes, <i>E(spl)m6-, m4-, m2-</i> and <i>mα-BFM</i> are intermingled and encode Notch repressor proteins of the Bearded-family (BFM). The complex is split by a single gene of unrelated function, encoding a Kazal-type protease inhibitor (<i>Kaz-m1</i>). All members within a family, bHLH-O or BFM, are very similar in structure and in function. In an attempt to generate specific mutants, we have mobilised P-element constructs residing next to <i>E(spl)m7-HLH</i> and <i>E(spl)mγ-HLH</i>, respectively. The resulting deletions were mapped molecularly and by cytology. Two small deletions affected only <i>E(spl)m7-HLH</i> and <i>E(spl)mδ</i>. The deficient flies were viable without apparent phenotype. Larger deletions, generated also by X-ray mutagenesis, uncover most of the <i>E(spl)-C</i>. The phenotypes of homozygous deficient embryos were analysed to characterize the respective loss of Notch signalling activity.</p>","PeriodicalId":2,"journal":{"name":"ACS Applied Bio Materials","volume":null,"pages":null},"PeriodicalIF":4.6000,"publicationDate":"2015-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/hrd2.00065","citationCount":"5","resultStr":"{\"title\":\"Deletion mapping in the Enhancer of split complex\",\"authors\":\"Elisa Wurmbach, Anette Preiss\",\"doi\":\"10.1111/hrd2.00065\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p>The <i>Enhancer of split complex [E(spl)-C]</i> comprises twelve genes of different classes. Seven genes encode proteins of with a basic-helix-loop-helix-orange (bHLH-O) domain that function as transcriptional repressors and serve as effectors of the Notch signalling pathway. They have been named <i>E(spl)m8-, m7-, m5-, m3-, mβ-, mγ-</i> and <i>mδ-HLH</i>. Four genes, <i>E(spl)m6-, m4-, m2-</i> and <i>mα-BFM</i> are intermingled and encode Notch repressor proteins of the Bearded-family (BFM). The complex is split by a single gene of unrelated function, encoding a Kazal-type protease inhibitor (<i>Kaz-m1</i>). All members within a family, bHLH-O or BFM, are very similar in structure and in function. In an attempt to generate specific mutants, we have mobilised P-element constructs residing next to <i>E(spl)m7-HLH</i> and <i>E(spl)mγ-HLH</i>, respectively. The resulting deletions were mapped molecularly and by cytology. Two small deletions affected only <i>E(spl)m7-HLH</i> and <i>E(spl)mδ</i>. The deficient flies were viable without apparent phenotype. Larger deletions, generated also by X-ray mutagenesis, uncover most of the <i>E(spl)-C</i>. The phenotypes of homozygous deficient embryos were analysed to characterize the respective loss of Notch signalling activity.</p>\",\"PeriodicalId\":2,\"journal\":{\"name\":\"ACS Applied Bio Materials\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":4.6000,\"publicationDate\":\"2015-01-14\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1111/hrd2.00065\",\"citationCount\":\"5\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"ACS Applied Bio Materials\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1111/hrd2.00065\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"MATERIALS SCIENCE, BIOMATERIALS\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"ACS Applied Bio Materials","FirstCategoryId":"99","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1111/hrd2.00065","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"MATERIALS SCIENCE, BIOMATERIALS","Score":null,"Total":0}
The Enhancer of split complex [E(spl)-C] comprises twelve genes of different classes. Seven genes encode proteins of with a basic-helix-loop-helix-orange (bHLH-O) domain that function as transcriptional repressors and serve as effectors of the Notch signalling pathway. They have been named E(spl)m8-, m7-, m5-, m3-, mβ-, mγ- and mδ-HLH. Four genes, E(spl)m6-, m4-, m2- and mα-BFM are intermingled and encode Notch repressor proteins of the Bearded-family (BFM). The complex is split by a single gene of unrelated function, encoding a Kazal-type protease inhibitor (Kaz-m1). All members within a family, bHLH-O or BFM, are very similar in structure and in function. In an attempt to generate specific mutants, we have mobilised P-element constructs residing next to E(spl)m7-HLH and E(spl)mγ-HLH, respectively. The resulting deletions were mapped molecularly and by cytology. Two small deletions affected only E(spl)m7-HLH and E(spl)mδ. The deficient flies were viable without apparent phenotype. Larger deletions, generated also by X-ray mutagenesis, uncover most of the E(spl)-C. The phenotypes of homozygous deficient embryos were analysed to characterize the respective loss of Notch signalling activity.