AhR mediates the expansion and specification of HPs. (A) Schematic representation of pHAGE2 lentiviral reporter constructs that contain the mouse mammary tumor virus flanking the dioxin response element (MMTV-AhRRE-MMTV) driving the expression of NLS-dsRed (pHAGE2-MMTV-AhRRE-MMTV-NLS-dsRed-IRES-zsGreen) (B) Representative FACS analysis for AhRRE-dsRED in HPs infected with pHAGE2-MMTV-AhRRE-MMTV-NLS-dsRed-IRES-ZsGreen. Infected cells were untreated or treated with 5 μM of CH223191, or 0.4 μM of FICZ. (C) Representative flow cytometry dot plots of live vs dead cells (PI vs Hoechst) from day 15 HPs ± FICZ and/or CH223191. For these experiments, HPs were pretreated with the known AhR inhibitor CH223191 on day 6 before the addition of FICZ on day 7. (D) Graphical representation of experiments performed in panel C. For the live-cell gate, data are the average of 3 independent experiments ± SD: *P < .005. For the apoptotic cell gate, data are the average of 3 independent experiments ± SD: *P < .04. (E) Expression of CYP1B1 as detected by quantitative PCR of MEPs from panel C, normalized to β-actin. Data are the average of 3 independent experiments ± SD: *P < .005.