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背甲蛋白的转录活性受到GATA DNA结合结构域与果蝇u型基因编码的辅因子异源二聚化的负调控。

Transcriptional activity of pannier is regulated negatively by heterodimerization of the GATA DNA-binding domain with a cofactor encoded by the u-shaped gene of Drosophila.

作者信息

Haenlin M, Cubadda Y, Blondeau F, Heitzler P, Lutz Y, Simpson P, Ramain P

机构信息

Institut de Génétique et de Biologie Moléculaire et Cellulaire, Centre National de la Recherche Scientifique/Institut National de la Santé et de la Recherche Médicale/Université Louis Pasteur, 67404 Illkirch Cedex, France.

出版信息

Genes Dev. 1997 Nov 15;11(22):3096-108. doi: 10.1101/gad.11.22.3096.

Abstract

The genes pannier (pnr) and u-shaped (ush) are required for the regulation of achaete-scute during establishment of the bristle pattern in Drosophila. pnr encodes a protein belonging to the GATA family of transcription factors, whereas ush encodes a novel zinc finger protein. Genetic interactions between dominant pnr mutants bearing lesions situated in the amino-terminal zinc finger of the GATA domain and ush mutants have been described. We show here that both wild-type Pannier and the dominant mutant form activate transcription from the heterologous alpha globin promoter when transfected into chicken embryonic fibroblasts. Furthermore, Pnr and Ush are found to heterodimerize through the amino-terminal zinc finger of Pnr and when associated with Ush, the transcriptional activity of Pnr is lost. In contrast, the mutant pnr protein with lesions in this finger associates only poorly with Ush and activates transcription even when cotransfected with Ush. These interactions have been investigated in vivo by overexpression of the mutant and wild-type proteins. The results suggest an antagonistic effect of Ush on Pnr function and reveal a new mode of regulation of GATA factors during development.

摘要

在果蝇刚毛模式建立过程中,基因篮状(pnr)和U型(ush)对于achaete - scute的调控是必需的。pnr编码一种属于GATA转录因子家族的蛋白质,而ush编码一种新型锌指蛋白。已经描述了位于GATA结构域氨基末端锌指处有损伤的显性pnr突变体与ush突变体之间的遗传相互作用。我们在此表明,野生型篮状蛋白(Pannier)和显性突变形式在转染到鸡胚成纤维细胞中时,都能激活来自异源α珠蛋白启动子的转录。此外,发现Pnr和Ush通过Pnr的氨基末端锌指形成异二聚体,并且当与Ush结合时,Pnr的转录活性丧失。相反,在这个锌指中有损伤的突变型pnr蛋白与Ush的结合很差,即使与Ush共转染时也能激活转录。通过突变型和野生型蛋白的过表达在体内研究了这些相互作用。结果表明Ush对Pnr功能有拮抗作用,并揭示了发育过程中GATA因子调控的一种新模式。

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