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用一种新型的残迹构建体拮抗缺刻显示出缺刻在黑腹果蝇腿部、眼睛和视叶发育中的重要作用。

Antagonizing scalloped with a novel vestigial construct reveals an important role for scalloped in Drosophila melanogaster leg, eye and optic lobe development.

作者信息

Garg Ankush, Srivastava Ajay, Davis Monica M, O'Keefe Sandra L, Chow Leola, Bell John B

机构信息

Department of Biological Sciences, University of Alberta, Edmonton, Alberta T6G 2E9, Canada.

出版信息

Genetics. 2007 Feb;175(2):659-69. doi: 10.1534/genetics.106.063966. Epub 2006 Nov 16.

DOI:10.1534/genetics.106.063966
PMID:17110491
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1800616/
Abstract

Scalloped (SD), a TEA/ATTS-domain-containing protein, is required for the proper development of Drosophila melanogaster. Despite being expressed in a variety of tissues, most of the work on SD has been restricted to understanding its role and function in patterning the adult wing. To gain a better understanding of its role in development, we generated sd(47M) flip-in mitotic clones. The mitotic clones had developmental defects in the leg and eye. Further, by removing the VG domains involved in activation, we created a reagent (VGDeltaACT) that disrupts the ability of SD to form a functional transcription factor complex and produced similar phenotypes to the flip-in mitotic clones. The VGDeltaACT construct also disrupted adult CNS development. Expression of the VGDeltaACT construct in the wing alters the cellular localization of VG and produces a mutant phenotype, indicating that the construct is able to antagonize the normal function of the SD/VG complex. Expression of the protein:protein interaction portion of SD is also able to elicit similar phenotypes, suggesting that SD interacts with other cofactors in the leg, eye, and adult CNS. Furthermore, antagonizing SD in larval tissues results in cell death, indicating that SD may also have a role in cell survival.

摘要

扇贝状蛋白(SD)是一种含TEA/ATTS结构域的蛋白质,对黑腹果蝇的正常发育至关重要。尽管它在多种组织中表达,但关于SD的大多数研究都局限于了解其在成年果蝇翅膀图案形成中的作用和功能。为了更好地理解其在发育中的作用,我们构建了sd(47M)翻转插入有丝分裂克隆。这些有丝分裂克隆在腿部和眼睛出现发育缺陷。此外,通过去除参与激活的VG结构域,我们创建了一种试剂(VGDeltaACT),它破坏了SD形成功能性转录因子复合物的能力,并产生了与翻转插入有丝分裂克隆相似的表型。VGDeltaACT构建体还破坏了成年果蝇中枢神经系统的发育。在翅膀中表达VGDeltaACT构建体会改变VG的细胞定位并产生突变表型,表明该构建体能够拮抗SD/VG复合物的正常功能。表达SD的蛋白质:蛋白质相互作用部分也能引发相似的表型,这表明SD在腿部、眼睛和成年果蝇中枢神经系统中与其他辅因子相互作用。此外,在幼虫组织中拮抗SD会导致细胞死亡,这表明SD可能在细胞存活中也发挥作用。

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