{"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":55057,"journal":{"name":"Hereditas","volume":"151 6","pages":"159-168"},"PeriodicalIF":2.1000,"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\":55057,\"journal\":{\"name\":\"Hereditas\",\"volume\":\"151 6\",\"pages\":\"159-168\"},\"PeriodicalIF\":2.1000,\"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\":\"Hereditas\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1111/hrd2.00065\",\"RegionNum\":3,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"GENETICS & HEREDITY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Hereditas","FirstCategoryId":"99","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1111/hrd2.00065","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"GENETICS & HEREDITY","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.
期刊介绍:
For almost a century, Hereditas has published original cutting-edge research and reviews. As the Official journal of the Mendelian Society of Lund, the journal welcomes research from across all areas of genetics and genomics. Topics of interest include human and medical genetics, animal and plant genetics, microbial genetics, agriculture and bioinformatics.