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Developmental Profiling of Tropomyosin Expression in Mouse Brain Reveals Tpm4.2 as the Major Post-synaptic Tropomyosin in the Mature Brain
Nerve cell connections, formed in the developing brain of mammals, undergo a well-programmed process of maturation with changes in their molecular composition over time. The major structural element at the post-synaptic specialization is the actin cytoskeleton, which is composed of different populat...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5743921/ https://www.ncbi.nlm.nih.gov/pubmed/29311841 http://dx.doi.org/10.3389/fncel.2017.00421 |
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author | Suchowerska, Alexandra K. Fok, Sandra Stefen, Holly Gunning, Peter W. Hardeman, Edna C. Power, John Fath, Thomas |
author_facet | Suchowerska, Alexandra K. Fok, Sandra Stefen, Holly Gunning, Peter W. Hardeman, Edna C. Power, John Fath, Thomas |
author_sort | Suchowerska, Alexandra K. |
collection | PubMed |
description | Nerve cell connections, formed in the developing brain of mammals, undergo a well-programmed process of maturation with changes in their molecular composition over time. The major structural element at the post-synaptic specialization is the actin cytoskeleton, which is composed of different populations of functionally distinct actin filaments. Previous studies, using ultrastructural and light imaging techniques have established the presence of different actin filament populations at the post-synaptic site. However, it remains unknown, how these different actin filament populations are defined and how their molecular composition changes over time. In the present study, we have characterized changes in a core component of actin filaments, the tropomyosin (Tpm) family of actin-associated proteins from embryonal stage to the adult stage. Using biochemical fractionation of mouse brain tissue, we identified the tropomyosin Tpm4.2 as the major post-synaptic Tpm. Furthermore, we found age-related differences in the composition of Tpms at the post-synaptic compartment. Our findings will help to guide future studies that aim to define the functional properties of actin filaments at different developmental stages in the mammalian brain. |
format | Online Article Text |
id | pubmed-5743921 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-57439212018-01-08 Developmental Profiling of Tropomyosin Expression in Mouse Brain Reveals Tpm4.2 as the Major Post-synaptic Tropomyosin in the Mature Brain Suchowerska, Alexandra K. Fok, Sandra Stefen, Holly Gunning, Peter W. Hardeman, Edna C. Power, John Fath, Thomas Front Cell Neurosci Neuroscience Nerve cell connections, formed in the developing brain of mammals, undergo a well-programmed process of maturation with changes in their molecular composition over time. The major structural element at the post-synaptic specialization is the actin cytoskeleton, which is composed of different populations of functionally distinct actin filaments. Previous studies, using ultrastructural and light imaging techniques have established the presence of different actin filament populations at the post-synaptic site. However, it remains unknown, how these different actin filament populations are defined and how their molecular composition changes over time. In the present study, we have characterized changes in a core component of actin filaments, the tropomyosin (Tpm) family of actin-associated proteins from embryonal stage to the adult stage. Using biochemical fractionation of mouse brain tissue, we identified the tropomyosin Tpm4.2 as the major post-synaptic Tpm. Furthermore, we found age-related differences in the composition of Tpms at the post-synaptic compartment. Our findings will help to guide future studies that aim to define the functional properties of actin filaments at different developmental stages in the mammalian brain. Frontiers Media S.A. 2017-12-22 /pmc/articles/PMC5743921/ /pubmed/29311841 http://dx.doi.org/10.3389/fncel.2017.00421 Text en Copyright © 2017 Suchowerska, Fok, Stefen, Gunning, Hardeman, Power and Fath. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Neuroscience Suchowerska, Alexandra K. Fok, Sandra Stefen, Holly Gunning, Peter W. Hardeman, Edna C. Power, John Fath, Thomas Developmental Profiling of Tropomyosin Expression in Mouse Brain Reveals Tpm4.2 as the Major Post-synaptic Tropomyosin in the Mature Brain |
title | Developmental Profiling of Tropomyosin Expression in Mouse Brain Reveals Tpm4.2 as the Major Post-synaptic Tropomyosin in the Mature Brain |
title_full | Developmental Profiling of Tropomyosin Expression in Mouse Brain Reveals Tpm4.2 as the Major Post-synaptic Tropomyosin in the Mature Brain |
title_fullStr | Developmental Profiling of Tropomyosin Expression in Mouse Brain Reveals Tpm4.2 as the Major Post-synaptic Tropomyosin in the Mature Brain |
title_full_unstemmed | Developmental Profiling of Tropomyosin Expression in Mouse Brain Reveals Tpm4.2 as the Major Post-synaptic Tropomyosin in the Mature Brain |
title_short | Developmental Profiling of Tropomyosin Expression in Mouse Brain Reveals Tpm4.2 as the Major Post-synaptic Tropomyosin in the Mature Brain |
title_sort | developmental profiling of tropomyosin expression in mouse brain reveals tpm4.2 as the major post-synaptic tropomyosin in the mature brain |
topic | Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5743921/ https://www.ncbi.nlm.nih.gov/pubmed/29311841 http://dx.doi.org/10.3389/fncel.2017.00421 |
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