Transcription factor E93 regulates wing development by directly promoting Dpp signaling in Drosophila

被引:10
|
作者
Wang, Weina [1 ]
Peng, Jian [1 ]
Li, Zheng [1 ]
Wang, Peng [1 ]
Guo, Mengpei [1 ]
Zhang, Tianlei [1 ]
Qian, Wenliang [1 ]
Xia, Qingyou [1 ,2 ]
Cheng, Daojun [1 ,2 ]
机构
[1] Southwest Univ, Biol Sci Res Ctr, State Key Lab Silkworm Genome Biol, Chongqing 400715, Peoples R China
[2] Southwest Univ, Chongqing Engn & Technol Res Ctr Novel Silk Mat, Chongqing Key Lab Sericultural Sci, Chongqing 400715, Peoples R China
基金
中国国家自然科学基金;
关键词
Drosophila; E93; Wing development; Dpp signaling; Transcriptional regulation; MORPHOGEN GRADIENTS; GENE; METAMORPHOSIS; PHOSPHORYLATION; CHROMATIN; LESSONS; PACKAGE; GROWTH;
D O I
10.1016/j.bbrc.2019.03.100
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Transcription factor E93 is a steroid hormone ecdysone early response gene and plays crucial roles in both the degradation of larval tissues and the formation of adult organs during insect metamorphosis with the prepupal-pupal-adult transition. However, the molecular mechanism underlying E93 regulation is poorly understood. In this study, we found that specific knockdown of the E93 gene in the Drosophila wing disrupted wing development. Analyzing ChIP-seq signals for E93 in Drosophila wing identified that the decapentaplegic (Dpp) gene was a potential downstream target of E93. Ch1P-PCR analysis and dual-luciferase reporter assay confirmed that E93 could bind to the Dpp promoter and enhanced its activity. Furthermore, the expressions of Dpp and other components in the Dpp signaling pathway were upregulated following E93 overexpression in Drosophila S2 cells but were decreased after E93 knockdown in the wing. Moreover, the impairment of the Dpp signaling pathway phenocopied the defects of E93 knockdown on wing development. Taken together, our results suggest that E93 modulates the Dpp signaling pathway to regulate wing development during Drosophila metamorphosis. (C) 2019 Elsevier Inc. All rights reserved.
引用
收藏
页码:280 / 286
页数:7
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