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转录因子Broad对成虫表皮基因Acp65A调控的解析

Elucidation of the regulation of an adult cuticle gene Acp65A by the transcription factor Broad.

作者信息

Cui H-Y, Lestradet M, Bruey-Sedano N, Charles J-P, Riddiford L M

机构信息

Department of Biology, University of Washington, Seattle, WA, USA.

出版信息

Insect Mol Biol. 2009 Aug;18(4):421-9. doi: 10.1111/j.1365-2583.2009.00889.x. Epub 2009 Apr 24.

Abstract

Broad (BR), an ecdysone-inducible transcription factor, is a major determinant of the pupal stage. The misexpression of BR-Z1 isoform (BR-Z1) during adult development of Drosophila melanogaster prevents the expression of the adult cuticle protein 65A gene (Acp65A). We found that the proximal 237 bp of the 5' flanking region of Acp65A were sufficient to mediate this suppression. A targeted point mutation of a putative BR-Z1 response element (BRE) within this region showed that it was not involved. Drosophila hormone receptor-like 38 (DHR38) is required for Acp65A expression. We found that BR-Z1 repressed DHR38 expression and that BR's inhibition of Acp65A expression was rescued by exogenous expression of DHR38. Thus, BR-Z1 suppresses Acp65A expression by preventing the normal up-regulation of DHR38 at the time of adult cuticle formation.

摘要

Broad(BR)是一种蜕皮激素诱导型转录因子,是蛹期的主要决定因素。黑腹果蝇成虫发育过程中BR-Z1亚型(BR-Z1)的错误表达会阻止成虫表皮蛋白65A基因(Acp65A)的表达。我们发现,Acp65A 5'侧翼区域近端的237 bp足以介导这种抑制作用。该区域内一个假定的BR-Z1反应元件(BRE)的靶向点突变表明其并不参与其中。果蝇激素受体样38(DHR38)是Acp65A表达所必需的。我们发现BR-Z1抑制DHR38的表达,并且通过外源表达DHR38可挽救BR对Acp65A表达的抑制作用。因此,BR-Z1通过在成虫表皮形成时阻止DHR38的正常上调来抑制Acp65A的表达。

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