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An epigenetically inherited UV hyper-resistance phenotype in Saccharomyces cerevisiae
BACKGROUND: Epigenetics refers to inheritable phenotypic changes that occur in the absence of genetic alteration. Such adaptations can provide phenotypic plasticity in reaction to environmental cues. While prior studies suggest that epigenetics plays a role in the response to DNA damage, no direct d...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9392361/ https://www.ncbi.nlm.nih.gov/pubmed/35986361 http://dx.doi.org/10.1186/s13072-022-00464-5 |
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author | Reardon, Rachel M. Walsh, Amanda K. Larsen, Clairine I. Schmidberger, LauraAnn H. Morrow, Lillian A. Thompson, Adriane E. Wellik, Isabel M. Thompson, Jeffrey S. |
author_facet | Reardon, Rachel M. Walsh, Amanda K. Larsen, Clairine I. Schmidberger, LauraAnn H. Morrow, Lillian A. Thompson, Adriane E. Wellik, Isabel M. Thompson, Jeffrey S. |
author_sort | Reardon, Rachel M. |
collection | PubMed |
description | BACKGROUND: Epigenetics refers to inheritable phenotypic changes that occur in the absence of genetic alteration. Such adaptations can provide phenotypic plasticity in reaction to environmental cues. While prior studies suggest that epigenetics plays a role in the response to DNA damage, no direct demonstration of epigenetically inheritable processes have been described in this context. RESULTS: Here we report the identification of an epigenetic response to ultraviolet (UV) radiation in the baker’s yeast Saccharomyces cerevisiae. Cells that have been previously exposed to a low dosage of UV exhibit dramatically increased survival following subsequent UV exposure, which we refer to as UV hyper-resistance (UVHR). This phenotypic change persists for multiple mitotic generations, without any indication of an underlying genetic basis. Pre-exposed cells experience a notable reduction in the amount of DNA damage caused by the secondary UV exposure. While the mechanism for the protection is not fully characterized, our results suggest that UV-induced cell size increases and/or cell wall changes are contributing factors. In addition, we have identified two histone modifications, H3K56 acetylation and H3K4 methylation, that are important for UVHR, potentially serving as mediators of UV protective gene expression patterns, as well as epigenetic marks to propagate the phenotype across cell generations. CONCLUSIONS: Exposure to UV radiation triggers an epigenetically inheritable protective response in baker’s yeast that increases the likelihood of survival in response to subsequent UV exposures. These studies provide the first demonstration of an epigenetically inheritable dimension of the cellular response to DNA damage. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13072-022-00464-5. |
format | Online Article Text |
id | pubmed-9392361 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-93923612022-08-21 An epigenetically inherited UV hyper-resistance phenotype in Saccharomyces cerevisiae Reardon, Rachel M. Walsh, Amanda K. Larsen, Clairine I. Schmidberger, LauraAnn H. Morrow, Lillian A. Thompson, Adriane E. Wellik, Isabel M. Thompson, Jeffrey S. Epigenetics Chromatin Research BACKGROUND: Epigenetics refers to inheritable phenotypic changes that occur in the absence of genetic alteration. Such adaptations can provide phenotypic plasticity in reaction to environmental cues. While prior studies suggest that epigenetics plays a role in the response to DNA damage, no direct demonstration of epigenetically inheritable processes have been described in this context. RESULTS: Here we report the identification of an epigenetic response to ultraviolet (UV) radiation in the baker’s yeast Saccharomyces cerevisiae. Cells that have been previously exposed to a low dosage of UV exhibit dramatically increased survival following subsequent UV exposure, which we refer to as UV hyper-resistance (UVHR). This phenotypic change persists for multiple mitotic generations, without any indication of an underlying genetic basis. Pre-exposed cells experience a notable reduction in the amount of DNA damage caused by the secondary UV exposure. While the mechanism for the protection is not fully characterized, our results suggest that UV-induced cell size increases and/or cell wall changes are contributing factors. In addition, we have identified two histone modifications, H3K56 acetylation and H3K4 methylation, that are important for UVHR, potentially serving as mediators of UV protective gene expression patterns, as well as epigenetic marks to propagate the phenotype across cell generations. CONCLUSIONS: Exposure to UV radiation triggers an epigenetically inheritable protective response in baker’s yeast that increases the likelihood of survival in response to subsequent UV exposures. These studies provide the first demonstration of an epigenetically inheritable dimension of the cellular response to DNA damage. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13072-022-00464-5. BioMed Central 2022-08-20 /pmc/articles/PMC9392361/ /pubmed/35986361 http://dx.doi.org/10.1186/s13072-022-00464-5 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Research Reardon, Rachel M. Walsh, Amanda K. Larsen, Clairine I. Schmidberger, LauraAnn H. Morrow, Lillian A. Thompson, Adriane E. Wellik, Isabel M. Thompson, Jeffrey S. An epigenetically inherited UV hyper-resistance phenotype in Saccharomyces cerevisiae |
title | An epigenetically inherited UV hyper-resistance phenotype in Saccharomyces cerevisiae |
title_full | An epigenetically inherited UV hyper-resistance phenotype in Saccharomyces cerevisiae |
title_fullStr | An epigenetically inherited UV hyper-resistance phenotype in Saccharomyces cerevisiae |
title_full_unstemmed | An epigenetically inherited UV hyper-resistance phenotype in Saccharomyces cerevisiae |
title_short | An epigenetically inherited UV hyper-resistance phenotype in Saccharomyces cerevisiae |
title_sort | epigenetically inherited uv hyper-resistance phenotype in saccharomyces cerevisiae |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9392361/ https://www.ncbi.nlm.nih.gov/pubmed/35986361 http://dx.doi.org/10.1186/s13072-022-00464-5 |
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