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The Trim family of genes and the retina: Expression and functional characterization
To better understand the mechanisms that govern the development of retinal neurons, it is critical to gain additional insight into the specific intrinsic factors that control cell fate decisions and neuronal maturation. In the developing mouse retina, Atoh7, a highly conserved transcription factor,...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6135365/ https://www.ncbi.nlm.nih.gov/pubmed/30208054 http://dx.doi.org/10.1371/journal.pone.0202867 |
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author | Chowdhury, Rebecca Laboissonniere, Lauren A. Wester, Andrea K. Muller, Madison Trimarchi, Jeffrey M. |
author_facet | Chowdhury, Rebecca Laboissonniere, Lauren A. Wester, Andrea K. Muller, Madison Trimarchi, Jeffrey M. |
author_sort | Chowdhury, Rebecca |
collection | PubMed |
description | To better understand the mechanisms that govern the development of retinal neurons, it is critical to gain additional insight into the specific intrinsic factors that control cell fate decisions and neuronal maturation. In the developing mouse retina, Atoh7, a highly conserved transcription factor, is essential for retinal ganglion cell development. Moreover, Atoh7 expression in the developing retina occurs during a critical time period when progenitor cells are in the process of making cell fate decisions. We performed transcriptome profiling of Atoh7+ individual cells isolated from mouse retina. One of the genes that we found significantly correlated with Atoh7 in our transcriptomic data was the E3 ubiquitin ligase, Trim9. The correlation between Trim9 and Atoh7 coupled with the expression of Trim9 in the early mouse retina led us to hypothesize that this gene may play a role in the process of cell fate determination. To address the role of Trim9 in retinal development, we performed a functional analysis of Trim9 in the mouse and did not detect any morphological changes in the retina in the absence of Trim9. Thus, Trim9 alone does not appear to be involved in cell fate determination or early ganglion cell development in the mouse retina. We further hypothesize that the reason for this lack of phenotype may be compensation by one of the many additional TRIM family members we find expressed in the developing retina. |
format | Online Article Text |
id | pubmed-6135365 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-61353652018-09-27 The Trim family of genes and the retina: Expression and functional characterization Chowdhury, Rebecca Laboissonniere, Lauren A. Wester, Andrea K. Muller, Madison Trimarchi, Jeffrey M. PLoS One Research Article To better understand the mechanisms that govern the development of retinal neurons, it is critical to gain additional insight into the specific intrinsic factors that control cell fate decisions and neuronal maturation. In the developing mouse retina, Atoh7, a highly conserved transcription factor, is essential for retinal ganglion cell development. Moreover, Atoh7 expression in the developing retina occurs during a critical time period when progenitor cells are in the process of making cell fate decisions. We performed transcriptome profiling of Atoh7+ individual cells isolated from mouse retina. One of the genes that we found significantly correlated with Atoh7 in our transcriptomic data was the E3 ubiquitin ligase, Trim9. The correlation between Trim9 and Atoh7 coupled with the expression of Trim9 in the early mouse retina led us to hypothesize that this gene may play a role in the process of cell fate determination. To address the role of Trim9 in retinal development, we performed a functional analysis of Trim9 in the mouse and did not detect any morphological changes in the retina in the absence of Trim9. Thus, Trim9 alone does not appear to be involved in cell fate determination or early ganglion cell development in the mouse retina. We further hypothesize that the reason for this lack of phenotype may be compensation by one of the many additional TRIM family members we find expressed in the developing retina. Public Library of Science 2018-09-12 /pmc/articles/PMC6135365/ /pubmed/30208054 http://dx.doi.org/10.1371/journal.pone.0202867 Text en © 2018 Chowdhury et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Article Chowdhury, Rebecca Laboissonniere, Lauren A. Wester, Andrea K. Muller, Madison Trimarchi, Jeffrey M. The Trim family of genes and the retina: Expression and functional characterization |
title | The Trim family of genes and the retina: Expression and functional characterization |
title_full | The Trim family of genes and the retina: Expression and functional characterization |
title_fullStr | The Trim family of genes and the retina: Expression and functional characterization |
title_full_unstemmed | The Trim family of genes and the retina: Expression and functional characterization |
title_short | The Trim family of genes and the retina: Expression and functional characterization |
title_sort | trim family of genes and the retina: expression and functional characterization |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6135365/ https://www.ncbi.nlm.nih.gov/pubmed/30208054 http://dx.doi.org/10.1371/journal.pone.0202867 |
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