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 Vegfa^120/120) 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 (Vegfa^120/120) (see Ruhrberg et al., 2002).