Growth factor that controls proliferation and cellular differentiation in the retina and bone formation. Plays a key role in regulating apoptosis during retinal development. Establishes dorsal-ventral positional information in the retina and controls the formation of the retinotectal map (PubMed:23307924). Required for normal formation of bones and joints in the limbs, skull, digits and axial skeleton. Plays a key role in establishing boundaries between skeletal elements during development. Regulation of GDF6 expression seems to be a mechanism for evolving species-specific changes in skeletal structures (PubMed:26774823). Seems to positively regulate differentiation of chondrogenic tissue through the growth factor receptors subunits BMPR1A, BMPR1B, BMPR2 and ACVR2A, leading to the activation of SMAD1-SMAD5-SMAD8 complex. The regulation of chondrogenic differentiation is inhibited by NOG (PubMed:12606286, PubMed:16049014). Also involved in the induction of adipogenesis from mesenchymal stem cells. This mechanism acts through the growth factor receptors subunits BMPR1A, BMPR2 and ACVR2A and the activation of SMAD1-SMAD5-SMAD8 complex and MAPK14/p38 (PubMed:23527555). Homodimer; disulfide-linked. Expressed in different subsets of developing joints. Highly expressed in the cochlea (PubMed:32369452). Strongly up-regulated in tibialis anterior muscles after denervation. Mice lacking GDF6 display photoreceptor degeneration. Animals exhibit abnormal electroretinograms with up to 66% decreases in the bipolar cell-driven b-wave and 54% decreases in the photoreceptor-mediated a-wave amplitudes, as well as 3 to 27% reduced photopic flicker fusion. The lengths, but not the widths, of dermal flat bones in the skull and the digits are significantly shorter than in wild type (PubMed:26774823). GDF6-knockout mice also shows cochlear aplasia, while the vestibular anatomy is normal (PubMed:32369452). Belongs to the TGF-beta family.