Targeted deletion of Tcf7l2 in adipocytes promotes adipocyte hypertrophy and impaired gluose metabolism [ChIP-seq]

We generated a Tcf7l2 F/F mouse and harvested preadipocytes rom these mice, immortalized them, and then transduced them with a retroviral vector containing CreERT2 and , differentiated them, performed ChIP-seq, and RNA-seq. We also generated and adipsoe specific knockout mouse where we crossed our Tcf7 F/Fmouse with an Adiponectin-Cre mice and performed RNA-seq on the inguimal white adipose tissue after 16 weeks of high fat diet, 65% Overall design: Examination of genome-wide TCF7L2 occupancy in wt and TCF7L2 deficient diiferentiated immortalized preadipocytes

我们构建了Tcf7l2 F/F小鼠，从该类小鼠中分离前体脂肪细胞（preadipocytes），对其进行永生化处理，随后用携带CreERT2的逆转录病毒载体（retroviral vector）进行转导，之后诱导细胞分化，分别开展染色质免疫共沉淀测序（ChIP-seq）与RNA测序（RNA-seq）。我们还构建了脂肪组织特异性敲除小鼠：将前述Tcf7l2 F/F小鼠与Adiponectin-Cre小鼠杂交，对喂食16周脂肪供能占比65%的高脂饲料后的小鼠腹股沟白色脂肪组织（inguinal white adipose tissue）进行RNA-seq。本数据集的整体设计为：检测野生型（wt）与TCF7L2缺陷的永生化分化前体脂肪细胞中全基因组范围内TCF7L2的结合占据情况。