IMAGE

Fig. 7

ID
ZDB-IMAGE-070924-10
Source
Figures for Chen et al., 2005
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Figure Caption

Fig. 7 HS6ST-2 and VEGF-A interact during caudal vein plexus formation in vivo. (A) Uninjected Tg(fli-1:EGFP) embryo at 33 hpf under FITC channel, with the inset displaying an enlargement of a segment in the venous plexus. (B) Embryo injected with 0.5 ng of HS6ST-2 MO2 displaying a venous plexus without any obvious defect. (C) Embryo injected with 1 ng of VEGF-A MO, displaying a venous plexus without any obvious defect. (D–E) Embryo co-injected with HS6ST-2 MO2 and VEGF-A MO displaying defective branching morphogenesis of the venous plexus as indicated by the formation of large loops (arrowheads in inset of D) and a single cavernous vessel with no branching (arrowheads in inset of E). The lines in A, D and E indicate regions in the venous plexus that are displayed in the insets. (F) A summary of two independent experiments is shown. Embryos co-injected with HS6ST-2 MO2 (0.5 ng) and VEGF-A MO (1 ng) exhibit a more than additive increase in the frequency (±SEM) of embryos with branching defects in the caudal vein plexus (column 3) compared to embryos injected with HS6ST-2 MO2 or VEGF-A MO only. In contrast, no synergy is observed in the embryos co-injected with HS6ST-2 MO and a four-base mismatch MO (d4, 1 ng) against VEGF-A (column 4).

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Reprinted from Developmental Biology, 284(2), Chen, E., Stringer, S.E., Rusch, M.A., Selleck, S.B., and Ekker, S.C., A unique role for 6-O sulfation modification in zebrafish vascular development, 364-376, Copyright (2005) with permission from Elsevier. Full text @ Dev. Biol.