Figure 6.

STAT5 activity can interact with FGF signaling in Xenopus embryos. Shown are representative embryos fixed and stained with benzidine to detect differentiated globin-expressing erythroid cells. Embryos had been injected into both blastomeres at the 2-cell stage with RNA encoding (A) lacZ as a control, (B) STAT5-EnR, (C) STAT5-VP16, (D) eFGF, (E) the dominant-negative FGFR isoform XFD, (F) eFGF + STAT5-EnR, (G) STAT5-VP16 + XFD. Benzidine-positive blood islands are indicated by the black arrows. Note that STAT5-VP16 and eFGF each inhibit VBI development (C-D). Restoring STAT5 repressor activity by STAT5-EnR is sufficient to rescue at least partially the repressive effect of eFGF (F), while XFD is unable to rescue VBI development that is repressed by STAT5-VP16 (G). Views are lateral with anterior to the left. The patterns shown were reproducible in at least 3 independent experiments. The embryos shown here are most representative of the staining patterns from one experiment representing the phenotype of (n) embryos: A, 12 of 19; B, 14 of 27; C, 12 of 12; D, 8 of 19; E, 23 of 26; F, 18 of 32; G, 21 of 29. (H) Shown is a representative Northern blot probed for RNA encoding embryonic α-globin (top panel) or as a loading control, the same blot reprobed for the housekeeping gene EF-1α (bottom panel). Samples are derived from pools of at least 25 embryos that had been injected with RNA encoding (1) lacZ as a control, (2) STAT5-VP16, (3) STAT5-EnR, (4) eFGF, (5) XFD, (6) eFGF + STAT5-EnR, (7) XFD + STAT5-VP16. Note that STAT5 repressor activity rescues much of the inhibition of globin transcription by eFGF (lane 6), while STAT5-VP16 is still partially repressive even in the presence of XFD (lane 7).