Bcar1/p130Cas is an important adaptor protein downstream of receptor tyrosine kinases, G-protein coupled receptors, and integrin signalling. It is required for the migration of endothelial cells and vascular smooth muscle cells in response to VEGF or PDGF stimulation in vitro. While global knockout causes embryonic lethality in the mouse due to severe cardiovascular defects, no further reports discuss its role in the cardiovascular system in vivo. To address this, we generated a novel knockout using the zebrafish model and used a combination of vascular reporters to interrogate p130Cas function during embryonic, regenerative and pathophysiological angiogenesis. We used confocal and light sheet microscopy to image live zebrafish embryos throughout development. A variety of transgenic vascular reporters, including the tg(fli1a:nEGFP)y7 line, allowed tracking of single endothelial cells. Unlike the mouse model, bcar1-/- zebrafish were viable and fertile, showing no gross morphological defects, neither in embryonic development nor adulthood. Furthermore, they were able to regenerate the caudal fin upon amputation. However, we observed a failure of venous endothelial cell sprouting and migration in p130Cas-deficient embryos in the caudal vein plexus starting from 26 hours post fertilisation (hpf) (see figure 01). This plexus resolved by 48hpf but maintained the reduced ventral extension already seen at 30hpf. We further observed a severe reduction in the development of the parachordal lymphangioblasts, the first lymphatic structures in the zebrafish trunk. P130Cas-deficient zebrafish embryos formed far fewer parachordal lymphangioblasts and these were also delayed in their migration (see figure 02). We present here a novel model for interrogating p130Cas function in vivo. While the zebrafish bcar1-/- mutant is not lethal, this allows investigation of more subtle effects in physiological and pathophysiological angiogenesis. We find a specific requirement for venous sprouting in the caudal vein plexus; this also impacts the initial development of the lymphatic system in the trunk. We are currently investigating other vascular beds dominated by venous sprouting and the signalling mechanism underlying this defect. Preliminary data shows increased phosphorylation of p130Cas in response to BMP2 treatment in vitro and we hypothesise that p130Cas could be a key downstream mediator of BMP signalling which is known to be an important regulator of venous angiogenesis Wiley et al. (2011).