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Figure 7


Fig. 7. Loss of SEMA3A does not rescue the vessel defects caused by the loss of heparin/neuropilin-binding VEGF isoforms. Visualisation (A-F) and quantitation (G) of vessel branching in 12.5 dpc mouse hindbrains derived from Sema3a+/- Vegfa+/120 matings. (A-F) PECAM-positive vessels in 0.25 mm2 areas of hindbrains expressing (Vegfa+/+) or lacking (Vegfa+/120 and Vegfa120/120) heparin/neuropilin-binding VEGF differed with respect to the presence (A-C) or absence (D-F) of SEMA3A. (G) Data from hindbrains expressing (Sema3a+/+) or lacking SEMA3A (Sema3a-/-) were grouped according to their level of VEGF isoform expression. Normal 12.5 dpc hindbrains express more VEGF164 than VEGF120 (Vegfa+/+); mutation of one Vegfa allele increases VEGF120 at the expense of VEGF164 (Vegfa+/120); mutation of both alleles ablates VEGF164 expression (Vegfa120/120) (see Ruhrberg et al., 2002).





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