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Artificially stimulating retrotransposon activity increases mortality and accelerates a subset of aging phenotypes in Drosophila
Transposable elements (TEs) are mobile sequences of DNA that can become transcriptionally active as an animal ages. Whether TE activity is simply a by-product of heterochromatin breakdown or can contribute toward the aging process is not known. Here, we place the TE gypsy under the control of the UA...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
eLife Sciences Publications, Ltd
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9427105/ https://www.ncbi.nlm.nih.gov/pubmed/35980024 http://dx.doi.org/10.7554/eLife.80169 |
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author | Rigal, Joyce Martin Anduaga, Ane Bitman, Elena Rivellese, Emma Kadener, Sebastian Marr, Michael T |
author_facet | Rigal, Joyce Martin Anduaga, Ane Bitman, Elena Rivellese, Emma Kadener, Sebastian Marr, Michael T |
author_sort | Rigal, Joyce |
collection | PubMed |
description | Transposable elements (TEs) are mobile sequences of DNA that can become transcriptionally active as an animal ages. Whether TE activity is simply a by-product of heterochromatin breakdown or can contribute toward the aging process is not known. Here, we place the TE gypsy under the control of the UAS GAL4 system to model TE activation during aging. We find that increased TE activity shortens the life span of male Drosophila melanogaster. The effect is only apparent in middle-aged animals. The increase in mortality is not seen in young animals. An intact reverse transcriptase is necessary for the decrease in life span, implicating a DNA-mediated process in the effect. The decline in life span in the active gypsy flies is accompanied by the acceleration of a subset of aging phenotypes. TE activity increases sensitivity to oxidative stress and promotes a decline in circadian rhythmicity. The overexpression of the Forkhead-box O family (FOXO) stress response transcription factor can partially rescue the detrimental effects of increased TE activity on life span. Our results provide evidence that active TEs can behave as effectors in the aging process and suggest a potential novel role for dFOXO in its promotion of longevity in D. melanogaster. |
format | Online Article Text |
id | pubmed-9427105 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | eLife Sciences Publications, Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-94271052022-08-31 Artificially stimulating retrotransposon activity increases mortality and accelerates a subset of aging phenotypes in Drosophila Rigal, Joyce Martin Anduaga, Ane Bitman, Elena Rivellese, Emma Kadener, Sebastian Marr, Michael T eLife Chromosomes and Gene Expression Transposable elements (TEs) are mobile sequences of DNA that can become transcriptionally active as an animal ages. Whether TE activity is simply a by-product of heterochromatin breakdown or can contribute toward the aging process is not known. Here, we place the TE gypsy under the control of the UAS GAL4 system to model TE activation during aging. We find that increased TE activity shortens the life span of male Drosophila melanogaster. The effect is only apparent in middle-aged animals. The increase in mortality is not seen in young animals. An intact reverse transcriptase is necessary for the decrease in life span, implicating a DNA-mediated process in the effect. The decline in life span in the active gypsy flies is accompanied by the acceleration of a subset of aging phenotypes. TE activity increases sensitivity to oxidative stress and promotes a decline in circadian rhythmicity. The overexpression of the Forkhead-box O family (FOXO) stress response transcription factor can partially rescue the detrimental effects of increased TE activity on life span. Our results provide evidence that active TEs can behave as effectors in the aging process and suggest a potential novel role for dFOXO in its promotion of longevity in D. melanogaster. eLife Sciences Publications, Ltd 2022-08-18 /pmc/articles/PMC9427105/ /pubmed/35980024 http://dx.doi.org/10.7554/eLife.80169 Text en © 2022, Rigal et al https://creativecommons.org/licenses/by/4.0/This article is distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use and redistribution provided that the original author and source are credited. |
spellingShingle | Chromosomes and Gene Expression Rigal, Joyce Martin Anduaga, Ane Bitman, Elena Rivellese, Emma Kadener, Sebastian Marr, Michael T Artificially stimulating retrotransposon activity increases mortality and accelerates a subset of aging phenotypes in Drosophila |
title | Artificially stimulating retrotransposon activity increases mortality and accelerates a subset of aging phenotypes in Drosophila |
title_full | Artificially stimulating retrotransposon activity increases mortality and accelerates a subset of aging phenotypes in Drosophila |
title_fullStr | Artificially stimulating retrotransposon activity increases mortality and accelerates a subset of aging phenotypes in Drosophila |
title_full_unstemmed | Artificially stimulating retrotransposon activity increases mortality and accelerates a subset of aging phenotypes in Drosophila |
title_short | Artificially stimulating retrotransposon activity increases mortality and accelerates a subset of aging phenotypes in Drosophila |
title_sort | artificially stimulating retrotransposon activity increases mortality and accelerates a subset of aging phenotypes in drosophila |
topic | Chromosomes and Gene Expression |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9427105/ https://www.ncbi.nlm.nih.gov/pubmed/35980024 http://dx.doi.org/10.7554/eLife.80169 |
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