| Annotated protein: | Ephrin type-A receptor 7 (EC 2.7.10.1) (Developmental kinase 1) (mDK-1) (EPH homology kinase 3) (EHK-3) (Embryonic brain kinase) (EBK). Gene symbol: EPHA7. Taxonomy: Mus musculus (Mouse). Uniprot ID: Q61772 |
| antibody wiki: | |
| SynGO gene info: | SynGO data @ EPHA7 |
| Ontology domain: | Biological Process |
| SynGO term: | regulation of postsynapse organization (GO:0099175) |
| Synapse type(s): | cerebral cortex, glutamatergic |
| Annotated paper: | Clifford MA, et al. "EphA7 signaling guides cortical dendritic development and spine maturation" Proc Natl Acad Sci U S A. 2014 Apr 1;111(13):4994-9 PMID:24707048 |
| Figure(s): | Fig 4, Fig. S3 and Fig 5C and D. |
| Annotation description: | Fig 4, in cortical neurons from EphA7-/- the number of dendritic protrusions is altered at P10 and P22 using Golgi staining. At P10, EphA7-/- neurons have more dendritic protrusions than WT neuron, at P22 EphA7-/- cortical neurons have fewer total protrusions, spines and filopodia than WT neurons. Literal: "Dendritic protrusions, filopodia, and spines were analyzed in WT and EphA7-/- neurons at two developmentally distinct ages: P10, when simple protrusions (filopodia) are prevalent and the development of dendritic spines is starting, and P22, when synaptic contacts have matured and protrusions have dendritic spine or filopodial morphology. At P10, WT cortical neurons extended 0.41 ± 0.011 protrusions/μm (Fig. 4A; black bar in Fig. 4C), and EphA7-/- neurons had significantly more protrusions (0.47 ± 0.016 protrusions/μm) (Fig. 4B; gray bar in Fig. 4C). Nevertheless, this result suggests that EphA7 acts to restrict dendritic protrusions early in postnatal life. Analysis at P22 revealed that WT neurons had 0.609 ± 0.014 protrusions/μm (Fig. 4D), most of which were dendritic spines (0.437 ± 0.033 spines/μm) (black arrowheads in Fig. 4) with a small proportion of filopodia (0.172 ± 0.003 filopodia/μm) (white arrowheads in Fig. 4). In contrast, EphA7-/- neurons had significantly fewer dendritic protrusions (0.237 ± 0.005 protrusions/μm) at P22, with a large proportion classified as dendritic spines (0.191 ± 0.017 spines/μm) and relatively few filopodia (0.046 ± 0.005 filopodia/μm) (Fig. 4E). The few dendritic protrusions seen in mature EphA7-/- neurons support a role for EphA7 in promoting both filopodia and spines in late postnatal life." Fig. S3, in cultured neurons from EphA7-/- KO mice the number of PSD-95 and GluA2 is reduced. Literal: "puncta of both PSD-95, a postsynaptic marker of mature excitatory synapses, and surface GluA2, the AMPA receptor subunit, were reduced in EphA7-/- cells compared with control neurons (Fig. S3). These results indicate that neurons from EphA7-/- mutant animals have fewer mature excitatory synaptic sites at DIV18 than do control neurons. Fig 5C and D, cultured neurons from EphA7-/- KO mice show delayed development of mESPCs in EphA7-/- cultured pyramidal neurons. Literal: "To examine the emergence of electrophysiological characteristics, the mEPSCs of pyramidal neurons in cultures through time were examined. For WT pyramidal neurons, the frequency of mEPSCs increased significantly from DIV14-18 and remained high at DIV21 (Fig. 5C, Left; white bar in Fig. 5D). In contrast, the frequency of mEPSCs was low at DIV14 and DIV18, with WT levels eventually achieved by DIV21 in EphA7-/-cultures (Fig. 5C, Right; gray bar in Fig. 5D, Upper Left). The frequency of mEPSCs was lower in EphA7-/- neurons than in WT neurons at DIV18 (Fig. 5D, Upper Left). However, no difference was observed between genotypes in the frequency of mEPSCs in fastspiking interneurons (Fig. 5D, Upper Right), and the amplitude of mEPSCs did not vary for based on cell type (Fig. 5C, Bottom)." |
| Evidence tracking, Biological System: | Intact tissue Cultured neurons |
| Evidence tracking, Protein Targeting: | Genetic transformation (eg; knockout, knockin, mutations) |
| Evidence tracking, Experiment Assay: | Microscopy (generic) Whole-cell patch clamp |
| Annotator(s): | Chiara Verpelli (ORCID:0000-0003-2949-9725) Carlo Sala (ORCID:0000-0003-0662-9523) |
| Lab: | CNR Neuroscience Institute Milan and Dept. of Biotechnology and Translational Medicine, University of Milan, 20129 Milan, Italy |
| SynGO annotation ID: | 1719 |
| Dataset release (version): | 20231201 |
| View annotation as GO-CAM model: |  |