Effect of depletion of Rictor on gene expression during 3% DSS treatment of colonic epithelial cells.

mTORC2 signaling is critical for maintaining cellular metabolic hemostasis. We here report mTORC2 as a key regulator of mitochondrial oxidative phosphorylation in colonic epithelial cells. The depletion of Rictor results in serious colitis after 5 days of DSS treatment. In addition, loss of Rictor impaired OXPHOS activity and ATP production. Taken together, our data provide a molecular framework for mTORC2 signaling in colonic inflammation, in which mTORC2 positively regulate mitochondrial OXPHOS activity. Overall design: To investigate mTORC2 signaling in the regulation of colitis, we generated Villin-Cre driven colonic epithelial conditional knockout Rictor mice (cKO), and induced colitis in both control and cKO mice by administering DSS in drinking water. We then performed gene expression profiling analysis using data obtained from RNA sequencing of colonic epithelial cells from control and cKO mice with or without DSS treatment. Comparation gene expression profiling analysis of RNA sequencing data for epithelial cells from control and cKO mice, epithelial cells from control and cKO mice after 3%DSS treatment, epithelial cells from normal water and 3% DSS treated mice.