| Type | disruption phenotype | Description | Mice show a reduced excitability attributed to inactivation of a fraction of brain glutamatergic synapses. At these synapses, vesicles are clustered and docked in normal numbers, but were unable to fuse. In retina, mutants lacking functional BSN showed normal retinal anatomy, but synapses lacked anchoring of the photoreceptor ribbon to the presynaptic active zone resulting in impaired photoreceptor synaptic transmission (PubMed:12628168). Knockdown of both Bassoon/BSN and Piccolo/PCLO leads to the formation of presynaptic autophagosomes. |
