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Epigenetic Control of Phenotypic Plasticity in the Filamentous Fungus Neurospora crassa
Phenotypic plasticity is the ability of a genotype to produce different phenotypes under different environmental or developmental conditions. Phenotypic plasticity is a ubiquitous feature of living organisms, and is typically based on variable patterns of gene expression. However, the mechanisms by...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Genetics Society of America
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5144970/ https://www.ncbi.nlm.nih.gov/pubmed/27694114 http://dx.doi.org/10.1534/g3.116.033860 |
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author | Kronholm, Ilkka Johannesson, Hanna Ketola, Tarmo |
author_facet | Kronholm, Ilkka Johannesson, Hanna Ketola, Tarmo |
author_sort | Kronholm, Ilkka |
collection | PubMed |
description | Phenotypic plasticity is the ability of a genotype to produce different phenotypes under different environmental or developmental conditions. Phenotypic plasticity is a ubiquitous feature of living organisms, and is typically based on variable patterns of gene expression. However, the mechanisms by which gene expression is influenced and regulated during plastic responses are poorly understood in most organisms. While modifications to DNA and histone proteins have been implicated as likely candidates for generating and regulating phenotypic plasticity, specific details of each modification and its mode of operation have remained largely unknown. In this study, we investigated how epigenetic mechanisms affect phenotypic plasticity in the filamentous fungus Neurospora crassa. By measuring reaction norms of strains that are deficient in one of several key physiological processes, we show that epigenetic mechanisms play a role in homeostasis and phenotypic plasticity of the fungus across a range of controlled environments. In general, effects on plasticity are specific to an environment and mechanism, indicating that epigenetic regulation is context dependent and is not governed by general plasticity genes. Specifically, we found that, in Neurospora, histone methylation at H3K36 affected plastic response to high temperatures, H3K4 methylation affected plastic response to pH, but H3K27 methylation had no effect. Similarly, DNA methylation had only a small effect in response to sucrose. Histone deacetylation mainly decreased reaction norm elevation, as did genes involved in histone demethylation and acetylation. In contrast, the RNA interference pathway was involved in plastic responses to multiple environments. |
format | Online Article Text |
id | pubmed-5144970 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Genetics Society of America |
record_format | MEDLINE/PubMed |
spelling | pubmed-51449702016-12-09 Epigenetic Control of Phenotypic Plasticity in the Filamentous Fungus Neurospora crassa Kronholm, Ilkka Johannesson, Hanna Ketola, Tarmo G3 (Bethesda) Investigations Phenotypic plasticity is the ability of a genotype to produce different phenotypes under different environmental or developmental conditions. Phenotypic plasticity is a ubiquitous feature of living organisms, and is typically based on variable patterns of gene expression. However, the mechanisms by which gene expression is influenced and regulated during plastic responses are poorly understood in most organisms. While modifications to DNA and histone proteins have been implicated as likely candidates for generating and regulating phenotypic plasticity, specific details of each modification and its mode of operation have remained largely unknown. In this study, we investigated how epigenetic mechanisms affect phenotypic plasticity in the filamentous fungus Neurospora crassa. By measuring reaction norms of strains that are deficient in one of several key physiological processes, we show that epigenetic mechanisms play a role in homeostasis and phenotypic plasticity of the fungus across a range of controlled environments. In general, effects on plasticity are specific to an environment and mechanism, indicating that epigenetic regulation is context dependent and is not governed by general plasticity genes. Specifically, we found that, in Neurospora, histone methylation at H3K36 affected plastic response to high temperatures, H3K4 methylation affected plastic response to pH, but H3K27 methylation had no effect. Similarly, DNA methylation had only a small effect in response to sucrose. Histone deacetylation mainly decreased reaction norm elevation, as did genes involved in histone demethylation and acetylation. In contrast, the RNA interference pathway was involved in plastic responses to multiple environments. Genetics Society of America 2016-09-29 /pmc/articles/PMC5144970/ /pubmed/27694114 http://dx.doi.org/10.1534/g3.116.033860 Text en Copyright © 2016 Kronholm et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article 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 the original work is properly cited. |
spellingShingle | Investigations Kronholm, Ilkka Johannesson, Hanna Ketola, Tarmo Epigenetic Control of Phenotypic Plasticity in the Filamentous Fungus Neurospora crassa |
title | Epigenetic Control of Phenotypic Plasticity in the Filamentous Fungus Neurospora crassa |
title_full | Epigenetic Control of Phenotypic Plasticity in the Filamentous Fungus Neurospora crassa |
title_fullStr | Epigenetic Control of Phenotypic Plasticity in the Filamentous Fungus Neurospora crassa |
title_full_unstemmed | Epigenetic Control of Phenotypic Plasticity in the Filamentous Fungus Neurospora crassa |
title_short | Epigenetic Control of Phenotypic Plasticity in the Filamentous Fungus Neurospora crassa |
title_sort | epigenetic control of phenotypic plasticity in the filamentous fungus neurospora crassa |
topic | Investigations |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5144970/ https://www.ncbi.nlm.nih.gov/pubmed/27694114 http://dx.doi.org/10.1534/g3.116.033860 |
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