RNA-sequencing shows the changes on transcriptomes after deletion of Setd2 in mice.

To explore a possible role of SETD2 in kidney development and tumorigenesis in vivo, we generated Setd2-floxed mice and deleted the Setd2 gene in tubular epithelial cells using a transgenic Ksp1.3/Cre mouse line. Then, we established our own c-MYC-transgene mouse line by overexpressing the human c-MYC under the control of the Ksp promoter to generate kidney disease mouse model. To get an insight into the mechanism of how SETD2 ablation promotes ccRCC formation in a c-MYC-generated PKD model, we performed RNA-seq using the renal tubules isolated from Wild Type, Setd2-KO, MYC-OE and MYC-OE; Setd2-KO mice. Overall design: Renal primary tubular epithelial cells mRNA profiles of three Wild Type mice, three Setd2-KO mice, three MYC-OE mice and three MYC-OE; Setd2-KO mice were generated by deep sequencing, in triplicate.