These transgenic mice express beta-galactosidase under the direction of the mouse Fabp4, fatty acid binding protein 4, adipocyte, (aP2) promoter. Beta-galactosidase activity is detected in transgenic embryos as early as 9.0 dpc in facial and eye ectoderm cells of the ventral region of brachial somites, and at age 10.5 dpc in myogenic cells, thymic epithelial precursors and nasal epithelium. In later stage embryos and in adult transgenic mice, beta-galactosidase activity is detected in the nuclei of vascular smooth muscle cells and pericytes (mural cells) of tissues such as the retina and skeletal muscle. No transgene expression is detected in major elastic arteries. For example, vascular smooth muscle cells of the coronary arteries from the proepicardial organ and intercostal arteries express the transgene, while the vascular smooth muscle cells of the ascending aorta and thoracic aorta do not. Transgene expression is not detected in skeletal and smooth muscles, the hepatic vascular bed and liver. During blood vessel injury, transgene expression is deactivated and is reactivated during would healing (formation of neointima thickening). Mice that are homozygous for the transgenic insert are viable and fertile. Preliminary results indicate that transgene expression in vascular smooth muscle cells could be driven by the 7.4 kb of upstream sequences of the promoter that is included in the transgenic construct.

In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.