| Annotated protein: | AP-1 complex subunit sigma-2 (Adaptor protein complex AP-1 subunit sigma-1B) (Adaptor-related protein complex 1 subunit sigma-1B) (Clathrin assembly protein complex 1 sigma-1B small chain) (Golgi adaptor HA1/AP1 adaptin sigma-1B subunit) (Sigma 1B subunit of AP-1 clathrin) (Sigma-adaptin 1B) (Sigma1B-adaptin). Gene symbol: AP1S2. Taxonomy: Mus musculus (Mouse). Uniprot ID: Q9DB50 |
| antibody wiki: | |
| SynGO gene info: | SynGO data @ AP1S2 |
| Ontology domain: | Biological Process |
| SynGO term: | synaptic vesicle budding from endosome (GO:0016182) |
| Synapse type(s): | hippocampus |
| Annotated paper: | Glyvuk N, et al. "AP-1/sigma1B-adaptin mediates endosomal synaptic vesicle recycling, learning and memory" EMBO J. 2010 Apr 21;29(8):1318-30 PMID:20203623 |
| Figure(s): | fig 4, fig 5 |
| Annotation description: | In figure 4 the authors demonstrate using AP-1 sigma1 KO mice that the number of SVs in the KO following a strong stimulation is dramatically reduced. The stimulation used is 900 AP/10 Hz. At this strength of stimulus, it is generally thought that the endocytosis of SV membranes and associated proteins occur via bulk endocytosis. In figure 5 they use synaptopHlourin to examine the endocytosis and recycling of a specific SV protein, synaptophysin. At weak stimulation (100 APs at 20 Hz ) there is only a slight delay in the internalization of synaptopHlourin as measured by acidification in the σ1B-deficient mice (Figure 5A). They then quantified SV recycling by measuring the rate of the recovery of the synaptopHluorin response after complete depletion of the total recycling SV pool (Figure 5C). They first applied a reference pulse (100 APs/20 Hz). They then applied a strong stimulus that completely depletes SVs (600 APs/50 Hz). Then, using different delay times, a second test pulse (100 APs/20 Hz) was given and the fraction of recovery was calculated as the paired pulse ratio of the two test pulse fluorescence amplitudes (ΔF2/ΔF1). Within the first 10 s after depleting stimulation, only 46.5% of the exocytosed vesicles become re-available for release in σ1B-deficient neurons compared with 94% in the isogenic controls. Moreover, SV reformation was incomplete in σ1B-deficient neurons, reaching only 70% (Figure 5C). These data demonstrate that the reduction in SV numbers determined in the EM images (figure 4) is caused by a defect in SV recycling. However, this is for AP-1 sigma 1.However, the AP-1 complex is an obligate heterotetramer and KO of sigma1 will lead to loss of beta1/mu1. |
| Evidence tracking, Biological System: | Cultured neurons |
| Evidence tracking, Protein Targeting: | Genetic transformation (eg; knockout, knockin, mutations) |
| Evidence tracking, Experiment Assay: | Electron Microscopy Optical physiology |
| Annotator(s): | Peter McPherson (ORCID:0000-0001-7806-5662) |
| Lab: | Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, Montreal, QC H3A 2B4, Canada |
| SynGO annotation ID: | 1633 |
| Dataset release (version): | 20231201 |
| View annotation as GO-CAM model: |  |