分裂复合体增强子中的删除映射

IF 2.1 3区 生物学 Q3 GENETICS & HEREDITY Hereditas Pub Date : 2015-01-14 DOI:10.1111/hrd2.00065
Elisa Wurmbach, Anette Preiss
{"title":"分裂复合体增强子中的删除映射","authors":"Elisa Wurmbach,&nbsp;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,&nbsp;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}
引用次数: 5

摘要

分裂复合体的增强子[E(spl)-C]由12个不同类别的基因组成。7个基因编码具有碱性螺旋-环-螺旋-橙色(bHLH-O)结构域的蛋白,其功能是转录抑制因子和Notch信号通路的效应器。它们被命名为E(spl)m8-、m7-、m5-、m3-、mβ-、mγ-和mδ-HLH。4个基因E(sp1)m6-、m4-、m2-和mα-BFM相互交织,编码BFM家族的Notch抑制蛋白。该复合体由一个功能不相关的基因分裂,该基因编码kazal型蛋白酶抑制剂(kazal -m1)。一个家族中的所有成员,bHLH-O或BFM,在结构和功能上都非常相似。为了产生特异性突变体,我们分别动员了位于E(spl)m7-HLH和E(spl)m - γ- hlh旁边的p元素构建体。由此产生的缺失被分子和细胞学定位。两个小的缺失只影响E(spl)m7-HLH和E(spl)mδ。有缺陷的果蝇可存活,无明显表型。较大的缺失,也由x射线诱变产生,揭示了大部分E(spl)-C。分析了纯合子缺陷胚胎的表型,以表征各自Notch信号活性的丧失。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

摘要图片

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
Deletion mapping in the Enhancer of split complex

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.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Hereditas
Hereditas 生物-遗传学
CiteScore
4.30
自引率
3.70%
发文量
46
审稿时长
6 weeks
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.
期刊最新文献
Trimeric complexes of Antp-TBP with TFIIEβ or Exd modulate transcriptional activity Insights into AIM-InDel diversities in Yunnan Miao and Hani ethnic groups of China for forensic and population genetic purposes. SKA3 is a prognostic biomarker and associated with immune infiltration in bladder cancer The Prevalence and Significance of Leukopenia Induced by Intravenous Iron Therapy in a Large Cohort of Females with Iron Deficiency Anemia (IDA). N6-methyladenosine-related lncRNAs is a potential marker for predicting prognosis and immunotherapy in ovarian cancer
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1