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. Author manuscript; available in PMC: 2024 Nov 6.
Published in final edited form as: Dev Cell. 2023 Oct 16;58(21):2206–2216.e5. doi: 10.1016/j.devcel.2023.09.005

Figure 3. Affinity-optimizing SNVs cause migration defects and disrupt heart development.

Figure 3.

A. Schematic showing a tailbud wild-type embryo, the concentration of activated ETS in the TVCs and ATMs and the role of FoxF in migration of the TVCs to the ventral midline. The TVCs have high levels of activated ETS while the ATMs have lower levels of activated ETS. FoxF enhancer drives expression of FoxF in the TVCs, causing them to migrate. B. Schematic showing a tailbud embryo containing the FoxF-ETS1-T-to-C enhancer driving FoxF. TVC cells have high levels of activated ETS, while ATMs have low levels of activated ETS. Embryos with the FoxF-ETS1-T-to-C enhancer drive expression of FoxF in the TVCs and ATMs causing the ATMs to express FoxF and migrate with the TVCs. C. Embryo with WT FoxF enhancer driving FoxF, co-electroporated with a MesP enhancer driving GFP marking the ATMs and TVCs at 16 hpf. D. Embryo with FoxF-ETS1-T-to-C enhancer driving FoxF, co-electroporated with a MesP enhancer driving GFP in the TVCs and ATMs at 16 hpf; all cells migrate to the ventral midline. Black cells in C and D are the otolith and ocellus. E. Juvenile with WT FoxF enhancer driving FoxF with heart colored in blue; normal heart morphology is seen. F. Juvenile with FoxF-ETS1-T-to-C enhancer driving FoxF has two hearts with main heart colored in pink, auxiliary heart colored in orange; abnormal heart morphology is seen in 79% (41/52) of embryos with migration defects. Hearts were false-colored digitally. G. Schematic of juvenile Ciona with normal heart morphology. H. Schematic of juvenile Ciona with auxiliary heart. Scale bars, 50 μm. See also Figure S4 and Movies S1,S2.