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Age‐associated de‐repression of retrotransposons in the Drosophila fat body, its potential cause and consequence
Eukaryotic genomes contain transposable elements (TE) that can move into new locations upon activation. Since uncontrolled transposition of TEs, including the retrotransposons and DNA transposons, can lead to DNA breaks and genomic instability, multiple mechanisms, including heterochromatin‐mediated...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4854910/ https://www.ncbi.nlm.nih.gov/pubmed/27072046 http://dx.doi.org/10.1111/acel.12465 |
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author | Chen, Haiyang Zheng, Xiaobin Xiao, Danqing Zheng, Yixian |
author_facet | Chen, Haiyang Zheng, Xiaobin Xiao, Danqing Zheng, Yixian |
author_sort | Chen, Haiyang |
collection | PubMed |
description | Eukaryotic genomes contain transposable elements (TE) that can move into new locations upon activation. Since uncontrolled transposition of TEs, including the retrotransposons and DNA transposons, can lead to DNA breaks and genomic instability, multiple mechanisms, including heterochromatin‐mediated repression, have evolved to repress TE activation. Studies in model organisms have shown that TEs become activated upon aging as a result of age‐associated deregulation of heterochromatin. Considering that different organisms or cell types may undergo distinct heterochromatin changes upon aging, it is important to identify pathways that lead to TE activation in specific tissues and cell types. Through deep sequencing of isolated RNAs, we report an increased expression of many retrotransposons in the old Drosophila fat body, an organ equivalent to the mammalian liver and adipose tissue. This de‐repression correlates with an increased number of DNA damage foci and decreased level of Drosophila lamin‐B in the old fat body cells. Depletion of the Drosophila lamin‐B in the young or larval fat body results in a reduction of heterochromatin and a corresponding increase in retrotransposon expression and DNA damage. Further manipulations of lamin‐B and retrotransposon expression suggest a role of the nuclear lamina in maintaining the genome integrity of the Drosophila fat body by repressing retrotransposons. |
format | Online Article Text |
id | pubmed-4854910 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-48549102016-06-16 Age‐associated de‐repression of retrotransposons in the Drosophila fat body, its potential cause and consequence Chen, Haiyang Zheng, Xiaobin Xiao, Danqing Zheng, Yixian Aging Cell Original Articles Eukaryotic genomes contain transposable elements (TE) that can move into new locations upon activation. Since uncontrolled transposition of TEs, including the retrotransposons and DNA transposons, can lead to DNA breaks and genomic instability, multiple mechanisms, including heterochromatin‐mediated repression, have evolved to repress TE activation. Studies in model organisms have shown that TEs become activated upon aging as a result of age‐associated deregulation of heterochromatin. Considering that different organisms or cell types may undergo distinct heterochromatin changes upon aging, it is important to identify pathways that lead to TE activation in specific tissues and cell types. Through deep sequencing of isolated RNAs, we report an increased expression of many retrotransposons in the old Drosophila fat body, an organ equivalent to the mammalian liver and adipose tissue. This de‐repression correlates with an increased number of DNA damage foci and decreased level of Drosophila lamin‐B in the old fat body cells. Depletion of the Drosophila lamin‐B in the young or larval fat body results in a reduction of heterochromatin and a corresponding increase in retrotransposon expression and DNA damage. Further manipulations of lamin‐B and retrotransposon expression suggest a role of the nuclear lamina in maintaining the genome integrity of the Drosophila fat body by repressing retrotransposons. John Wiley and Sons Inc. 2016-04-12 2016-06 /pmc/articles/PMC4854910/ /pubmed/27072046 http://dx.doi.org/10.1111/acel.12465 Text en © 2016 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd. This is an open access article under the terms of the Creative Commons Attribution (http://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Chen, Haiyang Zheng, Xiaobin Xiao, Danqing Zheng, Yixian Age‐associated de‐repression of retrotransposons in the Drosophila fat body, its potential cause and consequence |
title | Age‐associated de‐repression of retrotransposons in the Drosophila fat body, its potential cause and consequence |
title_full | Age‐associated de‐repression of retrotransposons in the Drosophila fat body, its potential cause and consequence |
title_fullStr | Age‐associated de‐repression of retrotransposons in the Drosophila fat body, its potential cause and consequence |
title_full_unstemmed | Age‐associated de‐repression of retrotransposons in the Drosophila fat body, its potential cause and consequence |
title_short | Age‐associated de‐repression of retrotransposons in the Drosophila fat body, its potential cause and consequence |
title_sort | age‐associated de‐repression of retrotransposons in the drosophila fat body, its potential cause and consequence |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4854910/ https://www.ncbi.nlm.nih.gov/pubmed/27072046 http://dx.doi.org/10.1111/acel.12465 |
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