READY TO SHIP!

IN PRODUCTION

Gdf6 is the mouse ortholog of human GDF6 and encodes BMP13, a ligand that signals through ALK3 and ALK6 with BMPR2 to activate SMAD1, SMAD5, and SMAD8, and that heterodimerizes with GDF5 to alter receptor preference and antagonist sensitivity. Its dominant requirement is ocular morphogenesis, where dosage controls optic fissure closure and retinal specification, explaining human microphthalmia with coloboma, Leber congenital amaurosis, and Klippel-Feil presentations, alongside segment-specific roles in wrist, ankle, and vertebral joint formation. Since nulls survive with restricted joint fusions and variable eye defects, conditional deletion is most useful for separating optic vesicle from periocular mesenchyme requirements, patient missense knockins test whether variants are hypomorphic or dominant negative through heterodimer poisoning, and humanization enables ligand trap and antibody pharmacology. Because Gdf5 and Gdf7 buffer overlapping skeletal domains, design compound conditional genetics early rather than reading a single-locus knockout as definitive.

A floxed Gdf6 allele paired with Cre gives spatial control that whole body knockouts cannot offer. People use it to separate developmental roles from adult homeostasis, to model somatic mutations, and to match disease that begins in one organ.