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Gene/Clone	Species	Stage	Anatomy Item	Experimenter
tnni3	xenopus

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Experiment details for tnni3

Fgf is required to regulate anterior-posterior patterning in the Xenopus lateral plate mesoderm.

Fgf is required to regulate anterior-posterior patterning in the Xenopus lateral plate mesoderm.

Gene	Clone	Species	Stages	Anatomy
tnni3.L		laevis	NF stage 28 to NF stage 29 and 30	heart , cardiac mesoderm , primary heart field , secondary heart field

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Fig. 2. Fgf is required for the patterning of late LPM markers. Hand1 (A and B) and foxf1 (C and D) are normally restricted in the anterior and middle LPM with a clear domain free of expression in both cases. When embryos are treated with SU5402, both hand1 (B) and foxf1 (D) are expressed along the entire anterior–posterior axis. Conversely, the LPM expression domains of both hoxc10 (E and F; normally expressed in the posterior half of the LPM) and tnni3 (G and H; marker of cardiac differentiation) are completely undetectable when Fgf signalling is inhibited. (A–F): lateral view of the embryos is shown, with anterior toward the left, dorsal at top. (G–H); ventral view of the heart region is shown, with anterior toward left. The total number of embryos examined for each panel is indicated in the lower left hand corner.

Gene	Clone	Species	Stages	Anatomy
tnni3.L		laevis	NF stage 28 to NF stage 29 and 30

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Supplementary Fig. 1. Inhibiting Vegf signalling with KRN633, a vegfr specific inhibitor does not recapitulate the SU5402 phenotype. Treating embryos with either 10 μM, or 25 μM KRN633 leads to a loss of angiogenesis when embryos are assayed for either etv2 (G–L) or aplnr (M–R) as demonstrated by a loss of vascular budding in the ventral trunk, and a loss of intersomitic vessels (white arrow heads). However, no concentration tested was able to block expression of tnni3 (A–F), or cause significant truncations of the tail.

Gene	Clone	Species	Stages	Anatomy
tnni3.L		laevis	NF stage 32	heart

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Fig. 4. Fgf signalling is necessary for heart patterning and morphogenesis. Embryos were treated with SU5402 during different developmental windows to determine when Fgf signalling is necessary for heart development and assayed for expression of nkx2.5 (A–D and I–L) or tnni3 (E–H and M–P). Fgf signalling was inhibited at successively later stages (top panel: A–H) and compared to control embryos (A and E). Embryos treated with SU5402 at either stage 12.5 (B and F) or stage 20 (C and G) demonstrate a complete loss of heart marker expression by stage 32, while embryos treated at stage 24 (D and H) show expression of both nkx2.5 and tnni3 but no discernable heart tube. Fgf signalling was also inhibited at stage 12.5 and restored at later stages by removing the inhibitor (bottom panel: I–P) and compared to control embryos (I and M). When Fgf signalling is restored by either stage 20 (J and N) or stage 22 (K and O), both heart markers are expressed however a normal heart tube is not formed. If signalling is not restored until stage 26 (L and P), neither nkx2.5 or tnni3 are detectable. White arrows mark the heart region. The total number of embryos examined for each panel is indicated in the lower left hand corner.

Gene	Clone	Species	Stages	Anatomy
tnni3.L		laevis	NF stage 32	heart

Supplementary Fig. 3. ATP promotes the efficacy of SU5402. (A) Embryos were treated with DMSO + ATP, 10 μM SU5402 or 10 μM SU5402 in conjunction with 0.1 mM ATP. Embryos treated with SU5402 alone elongated similar to DMSO controls, while embryos treated with SU5402 in conjunction with ATP demonstrate the truncated phenotype characteristic of a loss of FGF signalling. (B) Similar results are obtained when using cardiac differentiation, as assayed by expression of tnni3, although lower concentrations of SU5402 were effective. When embryos were exposed to 1 μM SU5402 alone cardiac differentiation was similar to controls but when embryos were exposed to 1 μM SU5402 in conjunction with 0.1 mM ATP, cardiac differentiation was blocked.