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. 2013 Mar 15;8(3):e58828. doi: 10.1371/journal.pone.0058828

Figure 3. Efficient excision of YY1 in definitive and visceral endoderm is accompanied by reduced HNF4α.

Figure 3

Immunofluorescence analysis of sectioned WT (A–D, I–K) and cKO tissue (E–H, L–N) at the stages indicated. A–C, I) YY1 (green) is ubiquitous in WT embryonic and extraembryonic tissues. A–B, D, K) HNF4α (red, orange when co-expressed with YY1) labels the visceral endoderm (A–B, D) and the developing liver bud (K). E–G, L) In cKO embryos, YY1 is downregulated in the extraembryonic visceral endoderm (VE) at 7.5 dpc (E) and is completely lost in the embryonic visceral endoderm by 8.75 dpc (F), when YY1 is also depleted in the definitive endoderm (DE) of the foregut. By 9.25 dpc YY1 is lost in most cells of the liver bud (L). E–F, H, N) Although HNF4α is present in the YY1-deficient visceral endoderm until 8.75 dpc (E, F) it is greatly reduced in both the visceral endoderm and in the nascent liver bud by 9.5 dpc. J, M) Despite the loss of YY1 in the nascent liver bud, the liver bud differentiation marker PROX1 is maintained in the cKO liver bud (M) at levels comparable to that observed in WT (J). The dotted line in C–D and G–H represent the division between the visceral endoderm and mesoderm derivative of the yolk sac, while in I–N the dashed line outlines the liver bud (LB).