*8.1. ADAM9*

ADAM9 (a disintegrin and metalloprotease domain, family member 9) mutations are associated with cone–rod dystrophies in humans and dogs. A genomic deletion in *Adam9* was identified in Irish Glen of Imaal Terriers, resulting in a premature stop codon and the loss of the full-length protein. Similar to the mouse model, histological sections show that the RPE cells do not invest in the outer segments of the photoreceptors. This mutation e ffects both the rod and cone photoreceptors, but the cones are more severely a ffected throughout the course of the disease [156,157]. Further work is needed to understand the role of ADAM9 in the retinal structure and RPE maintenance of photoreceptors.
