Previous studies have revealed that a mutation in a gene called ephrin-B1 caused abnormalities in facial development, but researchers were uncertain of how.
Bush, PhD, Postdoctoral Fellow, Developmental and Regenerative Biology, both at Mount Sinai School of Medicine, studied mice embryos that were genetically engineered to have a mutation in the ephrin-B1 gene.
They determined that ephrin-B1 controls craniofacial development by signaling cells to multiply and when there is a mutation in this gene, it causes anomalies in the cell proliferation process
For EphA7, EphB2, EphB4, EphB6, ephrin-B1, ephrin-B2, and ephrin-B3, immunohistochemistry was established to visualize some conclusive patterns of tissue-specific expression.
Immunohistochemistry was performed for EphA7, EphB2, EphB4, EphB6, ephrin-B1, ephrin-B2, and ephrinB3.
Ephrin-B1 transduces signals to activate integrin-mediated migration, attachment and angiogenesis.
The expression of ephrin B ligands in the callosal axons is suggestive of the involvement of reverse signaling, and Bush and Soriano showed that ephrin-B1 reverse signaling is critical for callosal axon pathfinding, which requires the binding of the PSD-95/Dlg/ZO-1 (PDZ) domain-containing proteins for the transduction of this reverse signal .
Soriano, "Ephrin-B1 regulates axon guidance by reverse signaling through a PDZ-dependent mechanism," Genes and Development, vol.