Mouse embryonic kidneys (E13.5): mutant (UB HDAC1,2-/-) vs. wild type

Transcriptional profiling of mouse embryonic kidneys (E13.5) comparing UB HDAC1,2-/- kidneys with wild type kidneys. Studies in our lab showed that histone deacetylase 1 (HDAC1) and 2 (HDAC2) perform redundant, yet essential functions in the developing mouse ureteric bud (UB) tissue. Double deletion of HDAC1 and HDAC2 in the UB results in impaired UB branching morphogenesis, followed by severe kidney dysgenesis. The goal of the microarray analysis was to identify the genetic pathways controlled by HDAC1 and 2 in the UB. Two-condition experiment: E13.5 mutant kidneys (UB HDAC1,2-/-) vs. E13.5 wild type kidneys . Biological replicates: 4 control replicates, 4 UB HDAC1,2-/- replicates. Two-color Agilent 4x44k chips with dye-swaps on 2 of 4 arrays.本数据集为小鼠胚胎肾脏（胚胎第13.5天，E13.5）的转录组分析，对比输尿管芽（Ureteric Bud，UB）HDAC1、2双敲除肾脏与野生型肾脏。本课题组前期研究证实，组蛋白去乙酰化酶1（HDAC1）与组蛋白去乙酰化酶2（HDAC2）在发育中小鼠输尿管芽（UB）组织中发挥功能冗余但不可或缺的作用。在UB中特异性敲除HDAC1与HDAC2，会导致UB分支形态发生受损，继而引发严重的肾脏发育不全。本次微阵列分析的核心目标为鉴定UB中受HDAC1与HDAC2调控的遗传通路。本实验为双条件对照设计：以E13.5 UB HDAC1、2双敲除突变肾脏与同胎龄野生型肾脏作为对比样本。生物学重复设置为：对照组与UB HDAC1、2双敲除组各设4次生物学重复。实验采用双色安捷伦（Agilent）4×44k基因芯片，且在4张芯片中的2张上开展了染料互换（dye-swap）操作。