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果蝇翅片上spalt基因表达受Decapentaplegic信号通路调控。

Regulation of spalt expression in the Drosophila wing blade in response to the Decapentaplegic signaling pathway.

作者信息

Barrio Rosa, de Celis Jose F

机构信息

Centro de Biología Molecular Severo Ochoa, Universidad Autónoma de Madrid, Cantoblanco, 28049 Madrid, Spain.

出版信息

Proc Natl Acad Sci U S A. 2004 Apr 20;101(16):6021-6. doi: 10.1073/pnas.0401590101. Epub 2004 Apr 12.

Abstract

Pattern formation depends on the acquisition of precise cellular identities due to the differential expression of transcription factors. Enhancers within regulatory regions integrate the positive and negative regulatory signals directing gene transcription. Here, we analyze the enhancer that drives expression of the Drosophila gene spalt in the wing blade. This enhancer integrates positive signals, mediated by the Decapentaplegic signaling effector protein Medea, with the repressor activity of Brinker. The enhancer functions in the absence of binding sites for the wing-specific factor Scalloped. The molecular analysis of this enhancer indicates that there are additional factors yet unknown involved in the activation of spalt in the wing blade and that the mechanism of repression by Brinker does not rely on competition with Mad-Medea overlapping sites. The comparisons with other enhancers that respond to Decapentaplegic suggest that there are different possibilities to integrate the positive and negative inputs triggered by this signaling pathway.

摘要

模式形成依赖于由于转录因子的差异表达而获得精确的细胞身份。调控区域内的增强子整合指导基因转录的正负调控信号。在这里,我们分析驱动果蝇基因spalt在翅片中表达的增强子。该增强子将由Decapentaplegic信号效应蛋白Medea介导的正信号与Brinker的抑制活性整合在一起。该增强子在没有翅特异性因子Scalloped结合位点的情况下发挥作用。对该增强子的分子分析表明,在翅片中激活spalt还涉及其他未知因子,并且Brinker的抑制机制不依赖于与Mad-Medea重叠位点的竞争。与其他对Decapentaplegic有反应的增强子的比较表明,整合该信号通路触发的正负输入有不同的可能性。

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