Synaptic AP2 CCV life cycle regulation by the Eps15, ITSN1, Sgip1/AP2, synaptojanin1 interactome.

ABSTRACT: The AP1/σ1B knockout causes impaired synaptic vesicle recycling and enhanced protein sorting into endosomes, leading to severe intellectual disability. These disturbances in synaptic protein sorting induce as a secondary phenotype the upregulation of AP2 CCV mediated endocytosis. Synapses contain canonical AP2 CCV and AP2 CCV with a more stable coat and thus extended life time. In AP1/σ1B knockout synapses, pool sizes of both CCV classes are doubled. Additionally, stable CCV of the knockout are more stabilised than stable wt CCV. One mechanism responsible for enhanced CCV stabilisation is the reduction of synaptojanin1 CCV levels, the PI-4,5-P₂ phosphatase essential for AP2 membrane dissociation. To identify mechanisms regulating synaptojanin1 recruitment, we compared synaptojan

SUBMITTER: Mishra R 

PROVIDER: S-EPMC8044098 | biostudies-literature | 2021 Apr

REPOSITORIES: biostudies-literature