F-Actin-Dependent Regulation of NESH Dynamics in Rat Hippocampal Neurons
Open accessAbstract
Synaptic plasticity is an important feature of neurons essential for learning and memory. Postsynaptic organization and composition are dynamically remodeled in response to diverse synaptic inputs during synaptic plasticity. During this process, the dynamics and localization of postsynaptic proteins are also precisely regulated. NESH/Abi-3 is a member of the Abl interactor (Abi) protein family. Overexpression of NESH is associated with reduced cell motility and tumor metastasis. Strong evidence of a close relationship between NESH and the actin cytoskeleton has been documented. Although earlier studies have shown that NESH is prominently expressed in the brain, its function and characteristics are yet to be established. Data from the present investigation suggest that synaptic localization of NESH in hippocampal neurons is regulated in an F-actin-dependent manner. The dynamic fraction of NESH in the dendritic spine was analyzed using FRAP (fluorescence recovery after photobleaching). Interestingly, F-actin stabilization and disruption significantly affected the mobile fraction of NESH, possibly through altered interactions of NESH with the F-actin. In addition, NESH was synaptically targeted from the dendritic shaft to spine after induction of chemical LTP (long-term potentiation) and the translocation was dependent on F-actin. Our data collectively support the significance of the F-actin cytoskeleton in synaptic targeting of NESH as well as its dynamics.
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ABI3 is mainly expressed in microglia, but its expression in neurons and interaction with filamentous actin in dendritic spines were observed in primary neuronal cell culture.
“Although ABI3 is mainly expressed in microglia, its expression in neurons and interaction with filamentous actin (F-actin) in dendritic spines were observed in primary neuronal cell culture (44, 63).”
From Deletion of <i>Abi3</i> gene locus exacerbates neuropathological features of Alzheimer’s disease in a mouse model of Aβ amyloidosis (2021) · cites this paper as [44]
The Methods describe primary rat hippocampal neuron cultures, and the Results report endogenous NESH/Abi-3 in neurons and its colocalization with F-actin in dendritic spines (page not available in our copy). The paper says NESH binds F-actin but labels that finding unpublished; it does not establish that ABI3 is mainly expressed in microglia. (LLM, conf=0.88)
Experimental — accuracy not yet measuredABI3 is involved in actin regulation.
“Because ABI3 is involved in actin regulation (13, 44), loss of Abi3 gene may impair actin remodeling and thereby migration of microglia toward Aβ plaques.”
From Deletion of <i>Abi3</i> gene locus exacerbates neuropathological features of Alzheimer’s disease in a mouse model of Aβ amyloidosis (2021) · cites this paper as [44]
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Karahan, H., Smith, D. C., Kim, B., Dabin, L. C., Al-Amin, M. M., Wijeratne, H. R. S., Pennington, T., Viana di Prisco, G., McCord, B., Lin, P. B.-C., et al. (2021) · Science Advances · doi:10.1126/sciadv.abe3954 · Cited by 53 · see citing works
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BackgroundThe NESH/Abi-3-based WAVE2 complex is functionally distinct from the Abi-1-based WAVE2 complex
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- Authors
- Bae, J., Sung, B. H., Cho, I. H., & Song, W. K.
- Affiliations
- Gwangju Institute of Science and Technology (KR)
- Vanderbilt University Medical Center (US)
- Corresponding author
- Song, Woo Keun
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2012-04-04
- Volume
- 7
- Issue
- 4
- Pages
- e34514
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3319579
- OpenAlex
- W2004171291
- Cited by
- 29
- References
- 5
- Citations by year
- 2025: 1 · 2024: 1 · 2022: 13 · 2021: 3 · 2020: 1 · 2019: 1 · 2018: 2 · 2017: 3 · 2016: 2 · 2015: 1 · 2014: 1
- FWCI
- 0.26
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Figshare (submittedVersion, cc-by)
- Funders
- National Research Foundation
- National Research Foundation of Korea
- Tokyo Medical and Dental University
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Keywords
- nesh, F-actin, actin cytoskeleton, hippocampal neurons, dendritic spines, synaptic plasticity, long-term potentiation, protein mobility, synaptic targeting
- MeSH terms
- Actins, Animals, Cells, Cultured, Female, Hippocampus, Image Processing, Computer-Assisted, Microfilament Proteins, Actin Cytoskeleton, Nerve Tissue Proteins, Neuronal Plasticity, Neurons, Synapses, Rats, Sprague-Dawley, Long-Term Potentiation, Protein Transport, Fluorescence Recovery After Photobleaching, Dendritic Spines, Rats
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