Extended Data Fig. 9: Acetylation-defective 6KR mutant MED1 promotes tumorigenesis and stress tolerance in a mouse model.
From: MED1 IDR deacetylation controls stress responsive genes through RNA Pol II recruitment
a, Measurement of tumor volume when mice bearing tumors of WT/KO or 6KR/KO MCF7 cells were sacrificed 133 or 95 days after implantation, respectively. Data are mean ± SEM. Number of tumors measured in each group is shown in parentheses. b, Immunoblotting showing comparable expression of HA-tagged (WT or 6KR) MED1 in WT/KO and 6KR/KO MCF7 tumors. Size-matched WT/KO and 6KR/KO MCF7 tumors were collected from NSG mice. Images with densitometry results (normalized by β-actin) are shown and plotted (right). c, Immunoblotting showing increased expression of NRF2 and NDRG1 in 6KR/KO versus WT/KO MCF7 tumors. Images with densitometry results (normalized by β-actin) are shown. d, e, Poly(A) RNA-seq for 6KR/KO and WT/KO MCF7 tumors developed in NSG mice. Three biological replicates were detected for each type of tumor. d, GSEA comparing the gene rank list with KEGG (left) and GOBP (right) pathway gene lists. Adjusted P values are noticed in addition to NES reported by bars. e, Fold change values of select stress-activated genes detected by RNA-seq. For b, c, each group has 3 tumors as biological replicates, the tests used the same samples, and the immunoblots are representative of three technical replicates. For a, b, the n.s. (no significance) indicates a p value > 0.05 (two-sided unpaired t-test).
