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. 2020 Sep 24;10:15589. doi: 10.1038/s41598-020-71753-w

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Src family kinases are required for caudal vein plexus formation. (A) Maximum intensity projections of wildtype embryos at 30hpf, exposed to DMSO control, PP2, or SU6656 inhibitors. Inhibition of Src family kinases caused defective CVP sprouting. Magenta dashed lines indicate the area of vascular front, shown below at higher magnification. Areas were inverted and contrast increased in FIJI for better visualisation. Magenta asterisks highlight filopodia-like protrusions. (B) Quantification of CVP area, number of endothelial gaps, total area of endothelial gaps, and number of filopodia-like cell protrusions showed significant reductions after inhibitor but not DMSO treatment. All results displayed as box plots with centre line showing median and box dimensions indicating 25th and 75th quartile. Each data point represents an individual embryo, experimental n from ≥ 3 independent experiments except for bcar1^u7000 PP2 which is n = 1, p values as shown. Scale bars as indicated.