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Disrupted-in-schizophrenia 1 (DISC1) and Syntaphilin collaborate to modulate axonal mitochondrial anchoring
In neuronal axons, the ratio of motile-to-stationary mitochondria is tightly regulated by neuronal activation, thereby meeting the need for local calcium buffering and maintaining the ATP supply. However, the molecular players and detailed regulatory mechanisms behind neuronal mitochondrial movement...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4930613/ https://www.ncbi.nlm.nih.gov/pubmed/27370822 http://dx.doi.org/10.1186/s13041-016-0250-2 |
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author | Park, Cana Lee, Seol-Ae Hong, Ji-Ho Suh, Yeongjun Park, Sung Jin Suh, Bo Kyoung Woo, Youngsik Choi, Jinhyuk Huh, Ji-Won Kim, You-Me Park, Sang Ki |
author_facet | Park, Cana Lee, Seol-Ae Hong, Ji-Ho Suh, Yeongjun Park, Sung Jin Suh, Bo Kyoung Woo, Youngsik Choi, Jinhyuk Huh, Ji-Won Kim, You-Me Park, Sang Ki |
author_sort | Park, Cana |
collection | PubMed |
description | In neuronal axons, the ratio of motile-to-stationary mitochondria is tightly regulated by neuronal activation, thereby meeting the need for local calcium buffering and maintaining the ATP supply. However, the molecular players and detailed regulatory mechanisms behind neuronal mitochondrial movement are not completely understood. Here, we found that neuronal activation-induced mitochondrial anchoring is regulated by Disrupted-in-schizophrenia 1 (DISC1), which is accomplished by functional association with Syntaphilin (SNPH). DISC1 deficiency resulted in reduced axonal mitochondrial movement, which was partially reversed by concomitant SNPH depletion. In addition, a SNPH deletion mutant lacking the sequence for interaction with DISC1 exhibited an enhanced mitochondrial anchoring effect than wild-type SNPH. Moreover, upon neuronal activation, mitochondrial movement was preserved by DISC1 overexpression, not showing immobilized response of mitochondria. Taken together, we propose that DISC1 in association with SNPH is a component of a modulatory complex that determines mitochondrial anchoring in response to neuronal activation. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13041-016-0250-2) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-4930613 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-49306132016-07-03 Disrupted-in-schizophrenia 1 (DISC1) and Syntaphilin collaborate to modulate axonal mitochondrial anchoring Park, Cana Lee, Seol-Ae Hong, Ji-Ho Suh, Yeongjun Park, Sung Jin Suh, Bo Kyoung Woo, Youngsik Choi, Jinhyuk Huh, Ji-Won Kim, You-Me Park, Sang Ki Mol Brain Research In neuronal axons, the ratio of motile-to-stationary mitochondria is tightly regulated by neuronal activation, thereby meeting the need for local calcium buffering and maintaining the ATP supply. However, the molecular players and detailed regulatory mechanisms behind neuronal mitochondrial movement are not completely understood. Here, we found that neuronal activation-induced mitochondrial anchoring is regulated by Disrupted-in-schizophrenia 1 (DISC1), which is accomplished by functional association with Syntaphilin (SNPH). DISC1 deficiency resulted in reduced axonal mitochondrial movement, which was partially reversed by concomitant SNPH depletion. In addition, a SNPH deletion mutant lacking the sequence for interaction with DISC1 exhibited an enhanced mitochondrial anchoring effect than wild-type SNPH. Moreover, upon neuronal activation, mitochondrial movement was preserved by DISC1 overexpression, not showing immobilized response of mitochondria. Taken together, we propose that DISC1 in association with SNPH is a component of a modulatory complex that determines mitochondrial anchoring in response to neuronal activation. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13041-016-0250-2) contains supplementary material, which is available to authorized users. BioMed Central 2016-07-02 /pmc/articles/PMC4930613/ /pubmed/27370822 http://dx.doi.org/10.1186/s13041-016-0250-2 Text en © The Author(s). 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Park, Cana Lee, Seol-Ae Hong, Ji-Ho Suh, Yeongjun Park, Sung Jin Suh, Bo Kyoung Woo, Youngsik Choi, Jinhyuk Huh, Ji-Won Kim, You-Me Park, Sang Ki Disrupted-in-schizophrenia 1 (DISC1) and Syntaphilin collaborate to modulate axonal mitochondrial anchoring |
title | Disrupted-in-schizophrenia 1 (DISC1) and Syntaphilin collaborate to modulate axonal mitochondrial anchoring |
title_full | Disrupted-in-schizophrenia 1 (DISC1) and Syntaphilin collaborate to modulate axonal mitochondrial anchoring |
title_fullStr | Disrupted-in-schizophrenia 1 (DISC1) and Syntaphilin collaborate to modulate axonal mitochondrial anchoring |
title_full_unstemmed | Disrupted-in-schizophrenia 1 (DISC1) and Syntaphilin collaborate to modulate axonal mitochondrial anchoring |
title_short | Disrupted-in-schizophrenia 1 (DISC1) and Syntaphilin collaborate to modulate axonal mitochondrial anchoring |
title_sort | disrupted-in-schizophrenia 1 (disc1) and syntaphilin collaborate to modulate axonal mitochondrial anchoring |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4930613/ https://www.ncbi.nlm.nih.gov/pubmed/27370822 http://dx.doi.org/10.1186/s13041-016-0250-2 |
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