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The Microbiological Memory, an Epigenetic Regulator Governing the Balance Between Good Health and Metabolic Disorders

If the transmission of biological information from one generation to the next is based on DNA, most heritable phenotypic traits such as chronic metabolic diseases, are not linked to genetic variation in DNA sequences. Non-genetic heritability might have several causes including epigenetic, parental...

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Autores principales: Devaux, Christian A., Raoult, Didier
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6028609/
https://www.ncbi.nlm.nih.gov/pubmed/29997595
http://dx.doi.org/10.3389/fmicb.2018.01379
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author Devaux, Christian A.
Raoult, Didier
author_facet Devaux, Christian A.
Raoult, Didier
author_sort Devaux, Christian A.
collection PubMed
description If the transmission of biological information from one generation to the next is based on DNA, most heritable phenotypic traits such as chronic metabolic diseases, are not linked to genetic variation in DNA sequences. Non-genetic heritability might have several causes including epigenetic, parental effect, adaptive social learning, and influence of the ecological environment. Distinguishing among these causes is crucial to resolve major phenotypic enigmas. Strong evidence indicates that changes in DNA expression through various epigenetic mechanisms can be linked to parent-offspring resemblance in terms of sensitivity to metabolic diseases. Among non-genetic heritable traits, early nutrition could account for a long term deviant programming of genes expression responsible for metabolic diseases in adulthood. Nutrition could shape an inadequate gut microbiota (dysbiosis), triggering epigenetic deregulation of transcription which can be observed in chronic metabolic diseases. We review herein the evidence that dysbiosis might be a major cause of heritable epigenetic patterns found to be associated with metabolic diseases. By taking into account the recent advances on the gut microbiome, we have aggregated together different observations supporting the hypothesis that the gut microbiota could promote the molecular crosstalk between bacteria and surrounding host cells which controls the pathological epigenetic signature. We introduce for the first time the concept of “microbiological memory” as the main regulator of the epigenetic signatures, thereby indicating that different causes of non-genetic heritability can interact in complex pathways to produce inheritance.
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spelling pubmed-60286092018-07-11 The Microbiological Memory, an Epigenetic Regulator Governing the Balance Between Good Health and Metabolic Disorders Devaux, Christian A. Raoult, Didier Front Microbiol Microbiology If the transmission of biological information from one generation to the next is based on DNA, most heritable phenotypic traits such as chronic metabolic diseases, are not linked to genetic variation in DNA sequences. Non-genetic heritability might have several causes including epigenetic, parental effect, adaptive social learning, and influence of the ecological environment. Distinguishing among these causes is crucial to resolve major phenotypic enigmas. Strong evidence indicates that changes in DNA expression through various epigenetic mechanisms can be linked to parent-offspring resemblance in terms of sensitivity to metabolic diseases. Among non-genetic heritable traits, early nutrition could account for a long term deviant programming of genes expression responsible for metabolic diseases in adulthood. Nutrition could shape an inadequate gut microbiota (dysbiosis), triggering epigenetic deregulation of transcription which can be observed in chronic metabolic diseases. We review herein the evidence that dysbiosis might be a major cause of heritable epigenetic patterns found to be associated with metabolic diseases. By taking into account the recent advances on the gut microbiome, we have aggregated together different observations supporting the hypothesis that the gut microbiota could promote the molecular crosstalk between bacteria and surrounding host cells which controls the pathological epigenetic signature. We introduce for the first time the concept of “microbiological memory” as the main regulator of the epigenetic signatures, thereby indicating that different causes of non-genetic heritability can interact in complex pathways to produce inheritance. Frontiers Media S.A. 2018-06-26 /pmc/articles/PMC6028609/ /pubmed/29997595 http://dx.doi.org/10.3389/fmicb.2018.01379 Text en Copyright © 2018 Devaux and Raoult. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Microbiology
Devaux, Christian A.
Raoult, Didier
The Microbiological Memory, an Epigenetic Regulator Governing the Balance Between Good Health and Metabolic Disorders
title The Microbiological Memory, an Epigenetic Regulator Governing the Balance Between Good Health and Metabolic Disorders
title_full The Microbiological Memory, an Epigenetic Regulator Governing the Balance Between Good Health and Metabolic Disorders
title_fullStr The Microbiological Memory, an Epigenetic Regulator Governing the Balance Between Good Health and Metabolic Disorders
title_full_unstemmed The Microbiological Memory, an Epigenetic Regulator Governing the Balance Between Good Health and Metabolic Disorders
title_short The Microbiological Memory, an Epigenetic Regulator Governing the Balance Between Good Health and Metabolic Disorders
title_sort microbiological memory, an epigenetic regulator governing the balance between good health and metabolic disorders
topic Microbiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6028609/
https://www.ncbi.nlm.nih.gov/pubmed/29997595
http://dx.doi.org/10.3389/fmicb.2018.01379
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