Dishevelled (Dvl) proteins are important signaling components of both the canonical β-catenin/Wnt pathway, which controls cell proliferation and patterning, migration, differentiation, stem cell renewal and the planar cell polarity (PCP) pathway. Mammals share three Dishevelled (Dvl) family members and while the roles of Dvl1 and Dvl2 have been described previously, the functions of Dvl3 have remained an area of active research. The lack of Dvl3 in mice affects the formation of the heart, neural tube, and inner ear and that the defects in these tissues are much more severe when the mice are deficient in more than one Dvl family member, indicating redundant functions for these genes. Congenital heart disease affects approximately 75 in every 1,000 live human births, and approximately 30% of these diseases are due to disruptions in the outflow tract, the region affected in mice lacking Dvl genes.
Homozygous embryos for this targeted mutation of dishevelled 3, dsh homolog (Drosophila) (Dvl3) exhibit cardiac conotruncal abnormalities such as persistent truncus arteriosis (PTA) and double outlet right ventricle (DORV), and cochlear defects (disoriented stereociliary bundles).
This mutant mouse strain may be useful in studies of cardiac development, neural tube formation and development of the inner ear.
The mice are designated Tangible Research Material (TRM). A complete description, including genotyping, phenotyping, etc is found at The Jackson Lab cat. No. 009083; https://www.jax.org/strain/009083
Academic and non-profit institutions please order directly from The Jackson Laboratory. Commercial entities require a license from UC San Diego contact ( https://innovation.ucsd.edu/contact/).
Dishevelled proteins, Dvl3 , mouse models, Wnt Pathway, Congenital heart disease