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. Author manuscript; available in PMC: 2018 Jan 10.
Published in final edited form as: Cell Rep. 2017 Jan 10;18(2):545–556. doi: 10.1016/j.celrep.2016.12.034

Figure 3. The C&E defects in Like1 morphants can be rescued by re-establishing smad2 signaling.

Figure 3

(A) Schematic of the morpholino employed to induce exon9 skipping (S2-i8e9-MO). (B) Immunoblotting of detergent extracts reveals a reduction in total and phospho-Smad2 protein expression in the S2-i8e9-morphants. (C–E) S2-i8e9-MO induction of smad2 mis-splicing phenocopied the C&E defects caused by Like1 knockdown, as indicated by altered morphology (C, red arrow) and alterations in ntl/hgg1/dlx3b and lefty1 expression and distribution, as measured by in situ hybridization (D, 10hpf, red arrows, anterior dorsal view; E, 16hpf, lateral view). (F–H) mRNA encoding constitutively activated smad2 (Ca-Smad2, 20pg) was utilized for injection alone or co-injected with Like1-A-MO. Embryo morphology (F) as well as the abnormal distribution of ntl (G, red arrows) and myod1 (H, red arrows) at 10hpf, can be rescued by ectopic expression of Ca-Smad2. All embryos are dorsal view with the anterior on top at 10hpf. All results are representative of at least 3 experiments performed. See also Figure S3.

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