Gene expression profiling on heads of Drosophila chromodomain helicase DNA binding protein 1 (CHD1) deletion mutants

CHD1 is a conserved ATP-dependent chromatin remodeling factor with roles in transcriptional regulation and chromatin assembly. Here we show that deletion of Chd1 causes multiple behavioral and metabolic defects. In particular, it diminishes food-intake and results in shortened lifespan of mutant flies. These phenotypes can be rescued by brain-specific expression of Chd1 via the elav promoter. Consistently, neuron-specific expression of Chd1 rescues the wide-spread transcriptional dysregulation observed in the absence of CHD1. Overall design: RNA was prepared from heads of 10 day-old Drosophila females for RNA-seq analysis. Three genoytypes were used (Chd1-deficient, Chd1-rescued, elavGal4>UAS-Chd1)

CHD1是一种保守的ATP依赖型染色质重塑因子（ATP-dependent chromatin remodeling factor），参与转录调控与染色质组装过程。本研究证实，Chd1基因缺失会引发多种行为与代谢缺陷：具体表现为进食量减少，并导致突变果蝇寿命缩短。上述异常表型可通过elav启动子介导的脑特异性Chd1表达得到挽救。一致性实验结果显示，在CHD1缺失的果蝇中，神经元特异性表达Chd1能够逆转广泛存在的转录失调现象。
实验整体设计：从10日龄雌性果蝇的头部提取RNA进行RNA测序（RNA-seq）分析，共设置三种基因型组别：Chd1缺陷型、Chd1挽救型、elavGal4>UAS-Chd1。