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. 2020 Sep 24;9:e54573. doi: 10.7554/eLife.54573

Figure 8. Inhibiting Hh signaling by GDC-0449 or Cyclopamine impairs PGC formation.

(A–D) The majority of primary polyps did not show visible developmental defects after treatment with GDC-0449 or Cyclopamine from the gastrula stage onward. (E–H) Primary polyps treated with GDC-0449 or Cyclopamine from 1 to 8 dpf formed significantly fewer PGCs than controls. p values of ANOVA tests were compared with control treatment. Scale bar = 50 µm in G. A-C are at the same scale; E–G are at the same scale.

Figure 8—source data 1. Quantification of normal primary polyps and aberrant development after GDC-0449 or Cyclopamine treatment.
Figure 8—source data 2. PGC numbers in GDC-0449 or Cyclopamine treated primary polyps.

Figure 8.

Figure 8—figure supplement 1. The Hh signaling pathway does not affect PGC behaviors after specification.

Figure 8—figure supplement 1.

(A) Design of Hh signaling inhibitor GDC-0449 treatments: 4 to 8 dpf larvae were tested for PGC specification, and 8 to 12 dpf polyps were tested for PGC behaviors post-specification. Ctrl: DMSO treatment. GDC: 25 µM GDC-0449 treatment. (B) Quantification of PGC numbers after treatments. During PGC specification (4–8 dpf), GDC-0449 resulted in significantly less PGC formation than control (analyzed by one-way ANOVA). After PGCs are specified (after 8 dpf), PGC number does not show significant difference among treatments. However, long-term treatment of DMSO resulted in significant side effects on the PGC number (compare Ctrl and Ctrl-Ctrl, p=0.02).
Figure 8—figure supplement 1—source data 1. PGC numbers in GDC-0449 treated 8 and 12 dpf primary polyps.