The ACTA2 gene encodes alpha smooth muscle actin; the most abundant protein in the vascular system. ACTA2 gene mutations are dominant negative mutations effecting protein function and interfering with the ability of arteries to adjust to the vascular load. Xenopus laevis is the right organism for the study because of its similarity with the human gene, being the (α)-2 actin 99% identical. Our goal is to understand how mutations in (α)-2 actin affect the development and function of the cardiovascular system. Using the ACTA2 promoter to guide the expression of a fluorescent protein while creating transgenic embryos. After the spatial and temporal activity of the promoter is established the characterized promoter will be used to control the expression of transgenes encoding ACTA2 mutations. The transgenesis efficiency was compared using four conformations of DNA; super coiled bacterial plasmid; PCR generated ACTA2 promoter with RFP; linear DNA with I-Sce-I and circularized DNA via the action of T4 DNA ligase. By developing transgenic embryos we observe the activity of the P2 ACTA2 promoter + RFP in the cardiovascular system and distinguish specific regions were the ACTA2 was expressed. The mosaic expression is due to either position effects or failure to integrate injected DNA into the genome. With this study we can conclude that to have a complete expression, the ACTA2 needs to be protected against position effects with insulators.  And we require more efficient integration. Insulators are DNA sequences that prevent position effects by establishing regulatory domains. The results were as expected, nevertheless, the model will be improved to enhance the expression within the embryos. It will be improved by optimizing the transgenic method, properly controlling the expression of the mutant actins and including mutations to the ACTA2 gene such as Thoracic Aortic Aneurysm and Dissection (TAAD).