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. 2018 Nov 19;145(22):dev165068. doi: 10.1242/dev.165068

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© 2018. Published by The Company of Biologists Ltd

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.

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Fig. 7. — Canonical signaling via Gli1 is required for coloboma in the ptch2^tc294z mutant. (A) Inhibition of non-canonical Hh signaling via Src-family kinases (SFKs) does not rescue coloboma in the ptch2^tc294z mutant. Graph shows percentage of ptch2^tc294z mutant embryos with coloboma, normalized to the DMSO control group. (B) Genetic loss of one or both copies of gli1 (using gli1^ts269) partially rescues the coloboma phenotype in the ptch2^tc294z mutant. Percentage of embryos with coloboma is shown. Numbers in parentheses indicate n. (C-F) Representative images of embryos from the genetic experiments shown in B, 55 hpf. (C) ptch2^+/−; gli1^any. (D) ptch2^−/−; gli1^+/+. (E) ptch2^−/−; gli1^+/−. (F) ptch2^−/−; gli1^−/−. Arrow indicates coloboma.