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. 2017 Oct 13;13(10):e1007047. doi: 10.1371/journal.pgen.1007047

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© 2017 Garg et al

This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Fig 3 — (A) FGF signaling target genes Etv1, Etv4 and Etv5 were expressed in the midbrain-hindbrain junction, branchial arches and nasal placode. These expressions patterns were significantly reduced by the deletions of Shp2 and Mek1/2 in the neural crest. Arrows point to Etv-expressing regions in the brain. (B) Lacrimal gland budding was lost in Wnt1-Cre; Mek1^f/f;Mek2^-/- and Wnt1-Cre; Erk1^-/-;Erk2^f/f mutants, but rescued by the constitutive activation of Ras signaling in Wnt1-Cre;Shp2^f/f;LSL-Kras^G12D embryos. Arrow: lacrimal gland primordia. (C) Wnt1-Cre mediated deletion of Etv1, 4 and 5 failed to disrupt lacrimal gland development. (D) Expression of the Etv4-Engrailed repressor (EnR) fusion protein in the neural crest led to craniofacial defects (arrow) and reduced lacrimal gland budding (arrowheads).