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. Author manuscript; available in PMC: 2018 Oct 4.
Published in final edited form as: Cell Rep. 2018 Aug 7;24(6):1434–1444.e7. doi: 10.1016/j.celrep.2018.07.009

Figure 3. Active ESR1 Fusions Promote Estrogen-Independent Expression of Target Genes.

Figure 3.

(A) Venn diagram depicting overlap of binding sites from hormone-deprived stable T47D cells expressing HA-tagged ESR1 constructs identified by HA-ChIP-seq.

(B) HA-ChIP followed by qPCR for ER-binding regions of ER-responsive genes and negative ER-binding region. Bar graphs show average values from three experiments ± SEM. Asterisks denote significant differences as described in STAR Methods.

(C) Heatmap showing differentially expressed genes near 445 sites bound by ESR1-e6>YAP1, ESR1-e6>PCDH11X, and ESR1-WT identified in (A). Known ER-responsive genes are indicated (CTSD, GREB1, PGR, TFF1, and PDZK1). Scale bar indicates row Z score.

(D) Bar graphs depicting relative fold changes of estrogen-responsive genes whose ER-binding regions were examined in (B) from hormone-deprived stable T47D cells, normalized to YFP −E2 (dark blue bar), after E2 addition (+E2, red bar), or in combination with fulvestrant (light blue and pink bars). −E2 and +E2 for ESR1 fusion-expressing cells have been omitted for clarity; see Figure S3F for complete data. Data are shown as averages from two independent experiments ± SEM.

See also Figure S3.