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. 2012 Jul 1;26(13):1445–1458. doi: 10.1101/gad.188193.112

Figure 6.

Figure 6.

Bmi1 promotes PrE emergence in a cell-autonomous manner. (A) Coimmunostainings for Bmi1, Gata6, and Gata4 were performed on agarose-embedded and microsectioned EBs cultured for 5 d. (B) Relative transcript levels for Bmi1, Oct3/4, Nanog, Gata6, Gata4, and Sox17 as assessed by qRT–PCR in control (ESControl) and Bmi1 knockdown (ESBmi1KD) ES cells upon EB formation for 5 d. Data were normalized to S17 and L19 and expressed relative to undifferentiated ESControl cells. Error bars represent the SD of two biological replicates. (C) Coimmunostainings for Gata6 and Gata4 performed on EBs cultured for 5 d in the presence (ESControl; top panel) or absence (ESBmi1KD; bottom panel) of Bmi1. Bars, 20 μM. (D) Schematic of chimeric EB formation. GFP-labeled ESControl or ESBmi1KD cells were mixed with unlabeled ESControl cells (ratio 1/1–1/3) and allowed to differentiate for 5 d upon EB formation. (E) Coimmunostainings for GFP and Gata6 performed on chimeric EBs formed as described in D. The outer layer of the EB structure is denoted by dotted lines. Bars, 20 μM.