Fig. 6: WDR18 association with PELP1 reduces ERα transcription coactivation.

a Endogenous co-IP of WDR18 from MCF7 cells treated with 10 nM E2 or ethanol. Western blot shows WDR18 interaction with PELP1 but not ERα. FT, flow through. co-IP and Western blot experiment in (a) was performed three times with reproducible results. b Dual luciferase assays in HepG2 cells treated with 10 nM E2 or ethanol showing ERα mediated transcription at a 3xERE promoter (n = 3 biologically independent samples per experiment). Overexpression of PELP1 induces robust transcriptional coactivation of ERα while WDR18 wild type and C-terminal deleted mutant (1-344aa) does not. Co-expression of PELP1 with WDR18 wild type prevents coactivation of ERα. Co-expression of PELP1 with WDR18 1-344aa regains ability for ERα coactivation due to impaired binding ability between PELP1 and WDR18 1-344aa. Independent experiments with n = 3 was performed three times with representative results shown. Statistics were determined using n from the one shown result. c Dual luciferase assays in MCF7 cells relying on endogenous ERα machinery with a similar experimental setup as in (b) (n = 4 biologically independent samples per experiment). Overexpression of PELP1 induces a detectable transcriptional coactivation of ERα while WDR18 wild-type overexpression alone reduces coactivation below empty vector control. Co-overexpression of PELP1 and WDR18 significantly reduces ERα coactivation below that of PELP1 overexpression alone. Independent experiments with n = 4 was performed two times with representative results shown. Statistics were determined using n from the one shown result. Source data are provided in the Source Data file.