DAG1 and neuromuscular disease caused by qualitative or quantitative defects of alpha-dystroglycan: Knockout of Dag1 after synapse formation in adult animals likewise causes selective loss of CCK terminals, but there is no such phenotype in the Dag1 T190M knock-in mouse – a model of α-dystroglycanopathy expressing a neurexin-binding-deficient αDG (Fruh et al., 2016).