Interaction with WDR5 promotes target gene recognition and tumorigenesis by MYC

We report a comparison of the genome-wide binding patterns of MYC and WDR5, and the effects of a mutation in MYC (WBM) that disrupt the MYC-WDR5 interaction. The experimental design included two distinct experimental strategies. For comparison of genome-wide binding patters of wild-type (WT) and WDR5 binding-deficient (WBM) MYC, HEK293 cells were engineered by retroviral transduction to express either FLAG-tagged WT-MYC, FLAG-tagged WBM-MYC, or an empty vector control ("vec") ChIP was performed on all samples using the anti-FLAG antibody, and co-precipitating DNAs subject to next-generation sequencing. Samples "2514-WPT-1_1", "2514-WPT-5_1" and "2514-WPT-13_1" are three independent biological replicates of ChIPs performed on the "vec" control cells (i.e., those not expressing any exogenous MYC). Samples "2514-WPT-2_1", "2514-WPT-6_1" and "2514-WPT-10_1" are three independent biological replicates of ChIPs performed on the WT-MYC expressing cells. "2514-WPT-3_1", "2514-WPT-7_1" and "2514-WPT-11_1" are three independent biological replicates of ChIPs performed on the WBM-MYC expressing cells. For comparison of these binding patterns with those of WDR5, we performed ChIP in HEK293 cells with either an antibody against WDR5, or with IgG (negative control). Samples "2514-WPT-23_1", "2514-WPT-25_1", and "2514-WPT-27_1" are independent biological replicates of ChIPs performed with the anti-WDR5 antibody. Samples "2514-WPT-24_1", "2514-WPT-26_1", and "2514-WPT-28_1" are independent biological replicates of ChIPs performed with the negative IgG control.