Materials and Methods.

Figs A-E. (A) Experimental design for gestational exposure to the prototypical AHR ligand (TCDD). (B) Body weight (grams) from naïve Ahr+/+, low- and high-dose ligand-exposed Ahr+/+, and Ahr-/- males and females at the indicated age (in days). Mean ± SEM. (C) Echocardiographic assessment of aorta diameter (μm) from naïve Ahr+/+, ligand-exposed Ahr+/+, and Ahr-/- males and females at the indicated age (in days). Mean ± SEM; * p≤0.05. (D) Mean blood pressure (mmHg) from naïve Ahr+/+, ligand-exposed Ahr+/+, and Ahr-/- males and females at 9 months (post natal day [PND] 270). Mean ± SEM; * p≤0.05. (E) RNA.seq data analysis design for adult heart transcriptome at PND 300 and comparison relative to embryo heart (i.e., persistent genes) transcriptome at either E13.5, E15.5, or E18.5. Table A: Identity of genes differentially expressed in the embryo at either E13.5, E15.5, or E18.5 which persisted in the adult hearts at post natal day (PND) 300. Table B: Identity, function, targets, and fate of selected cardiovascularsignaling pathways genes and proteins in cardiac hypertrophy and failure. Table C: Summary of cardiovascular findings related to developmental Ahr disruption in male and female mice. Arrow up = upregulated/increased, arrow down = downregulated/decreased, “↔” = not affected. (DOCX)