Annotated protein: | Pleckstrin and Sec7 domain containing. Gene symbol: PSD. Taxonomy: Rattus norvegicus (Rat). Uniprot ID: G3V8J5 |
antibody wiki: | |
SynGO gene info: | SynGO data @ PSD |
Ontology domain: | Biological Process |
SynGO term: | maintenance of postsynaptic density structure (GO:0099562) |
Synapse type(s): | hippocampus, glutamatergic |
Annotated paper: | Choi S, et al. "ARF6 and EFA6A regulate the development and maintenance of dendritic spines" J Neurosci. 2006 May 3;26(18):4811-9 PMID:16672654 |
Figure(s): | fig 3, 5, 8 |
Annotation description: | EFA6A protects mature dendritic spines from tetrodotoxin (inactivity)-induced destabilization in cultured hippocampal neurons. 21/2/2018 PIm Fig.3: "EFA6A promotes spine formation through ARF6 activation" - " Consistently, EFA6A E242K caused an increase in the length of dendritic protrusions and decreases in protrusion width and PSD-95 localization in spines (Fig. 3E-J). These results suggest that EFA6A promotes spine formation in an ARF6-dependent manner." [Fig.4: "The C-terminal (PH+C) region of EFA6A leads to an increase in spine density" - This is caused by an increase in formation of filopodia and is shown to be independent of ARF6.] Fig.4 is not in support of 'maturation' or 'maintenance' annotations Fig.5: "Knockdown of EFA6A and ARF6 by siRNA results in a decrease in spine formation" - Knockdown of ARF6 in cultured neurons (DIV 13-16) led to a decrease in spine density, with a concomitant increase in filopodia density (Fig. 5A-D), probably because of a reduced filopodia-to-spine conversion...Knockdown of EFA6A also resulted in similar changes, although to a lesser extent in some parameters, compared with ARF6 knockdown (Fig. 5A-J)." [Fig.6: "ARF6 is required for the conversion of filopodia to spines and stabilization of early spines" - " ARF6 knockdown markedly decreased the percentage of filopodia converted to spines (Fig. 6D), indicating that ARF6 is required for filopodia-to-spine conversion. When spines were monitored, ARF6 knockdown increased the percentage of spines disappeared but did not affect that converted to filopodia (Fig. 6E), indicating that ARF6 is required for the stabilization of early spines, in addition to filopodia-to-spine conversion. "] This figure does not relate to EFA6A Fig.8: "ARF6 and EFA6A protect mature spines from destabilization." - "neurons expressing ARF6 T157A or EFA6A (DIV 17-20) were resistant to TTX-induced elongation of spines, with complete protection seen in ARF6 T157A (Fig. 8A-F). These results suggest that ARF6 and EFA6A may be involved in the stabilization of mature spines at the later stages." Note: EFA6A is shown to act via ARF6. ARF6 and EFA6A are shown to: "In support of this, overexpression of an active form of ARF6 (T157A) promotes spine formation even at an early stage (DIV 11), whereas siRNA knockdown of ARF6 suppresses it. Critically, our live imaging results demonstrate that ARF6 is required for the conversion of filopodia to spines and stabilization of early spines. Active ARF6 (T157A) also causes a decrease in protrusion length and increases in protrusion width and spine localization of PSD-95, all of which may reflect a morphological maturation accompanying filopodia-to-spine conversion. Conversely, siRNA knockdown of ARF6 results in increased protrusion length and decreased protrusion width and spine localization of PSD-95. Last, ARF6 protects mature spines from TTX-induced destabilization." - Together, these data point to a role in formation and maintenance of PSD's |
Evidence tracking, Biological System: | Cultured neurons |
Evidence tracking, Protein Targeting: | RNAi / shRNA Over-expression |
Evidence tracking, Experiment Assay: | Confocal |
Annotator(s): | Hwajin Jung (ORCID:0000-0001-6194-9648) Eunjoon Kim (ORCID:0000-0001-5518-6584) |
Lab: | Center for Synaptic Brain Dysfunctions, Institute for Basic Science (IBS) and Department of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Daejeon 34141, South Korea |
SynGO annotation ID: | 2600 |
Dataset release (version): | 20231201 |
View annotation as GO-CAM model: |