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The mechanisms of epigenetic inheritance: How diverse are they? / Тиходеев, Олег Николаевич.

In: Biological Reviews, Vol. 93, No. 4, 11.2018, p. 1987-2005.

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@article{87b1c6f9ca154a40ab10f0a5e4190ba2,
title = "The mechanisms of epigenetic inheritance: How diverse are they?",
abstract = "Although epigenetic inheritance (EI) is a rapidly growing field of modern biology, it still has no clear place in fundamental genetic concepts which are traditionally based on the hereditary role of DNA. Moreover, not all mechanisms of EI attract the same attention, with most studies focused on DNA methylation, histone modification, RNA interference and amyloid prionization, but relatively few considering other mechanisms such as stable inhibition of plastid translation. Herein, we discuss all known and some hypothetical mechanisms that can underlie the stable inheritance of phenotypically distinct hereditary factors that lack differences in DNA sequence. These mechanisms include (i) regulation of transcription by DNA methylation, histone modifications, and transcription factors, (ii) RNA splicing, (iii) RNA-mediated post-transcriptional silencing, (iv) organellar translation, (v) protein processing by truncation, (vi) post-translational chemical modifications, (vii) protein folding, and (viii) homologous and non-homologous protein interactions. The breadth of this list suggests that any or almost any regulatory mechanism that participates in gene expression or gene-product functioning, under certain circumstances, may produce EI. Although the modes of EI are highly variable, in many epigenetic systems, stable allelic variants can be distinguished. Irrespective of their nature, all such alleles have an underlying similarity: each is a bimodular hereditary unit, whose features depend on (i) a certain epigenetic mark (epigenetic determinant) in the DNA sequence or its product, and (ii) the DNA sequence itself (DNA determinant; if this is absent, the epigenetic allele fails to perpetuate). Thus, stable allelic epigenetic inheritance (SAEI) does not contradict the hereditary role of DNA, but involves additional molecular mechanisms with no or almost no limitations to their variety.",
keywords = "epigenetic inheritance, DNA methylation, histone modification, chromatin remodelling, bistable gene networks, hereditary prions, RNA interference, self-splicing, trans-generation memory, body-to-body information transfer., epigenetic inheritance, DNA methylation, histone modification, chromatin remodelling, bistable gene networks, hereditary prions, RNA interference, self-splicing, trans-generation memory, body-to-body information transfer., body-to-body information transfer, DEOXYRIBONUCLEIC-ACID, POLYPEPTIDE-CHAIN, ARABIDOPSIS-THALIANA, SMALL RNAS, DNA METHYLATION, PODOSPORA-ANSERINA, GROUP-I INTRONS, YEAST SACCHAROMYCES-CEREVISIAE, GENE-EXPRESSION, TRANSGENERATIONAL INHERITANCE",
author = "Тиходеев, {Олег Николаевич}",
year = "2018",
month = nov,
doi = "doi: 10.1111/brv.12429",
language = "English",
volume = "93",
pages = "1987--2005",
journal = "Biological Reviews",
issn = "1464-7931",
publisher = "Cambridge University Press",
number = "4",

}

RIS

TY - JOUR

T1 - The mechanisms of epigenetic inheritance: How diverse are they?

AU - Тиходеев, Олег Николаевич

PY - 2018/11

Y1 - 2018/11

N2 - Although epigenetic inheritance (EI) is a rapidly growing field of modern biology, it still has no clear place in fundamental genetic concepts which are traditionally based on the hereditary role of DNA. Moreover, not all mechanisms of EI attract the same attention, with most studies focused on DNA methylation, histone modification, RNA interference and amyloid prionization, but relatively few considering other mechanisms such as stable inhibition of plastid translation. Herein, we discuss all known and some hypothetical mechanisms that can underlie the stable inheritance of phenotypically distinct hereditary factors that lack differences in DNA sequence. These mechanisms include (i) regulation of transcription by DNA methylation, histone modifications, and transcription factors, (ii) RNA splicing, (iii) RNA-mediated post-transcriptional silencing, (iv) organellar translation, (v) protein processing by truncation, (vi) post-translational chemical modifications, (vii) protein folding, and (viii) homologous and non-homologous protein interactions. The breadth of this list suggests that any or almost any regulatory mechanism that participates in gene expression or gene-product functioning, under certain circumstances, may produce EI. Although the modes of EI are highly variable, in many epigenetic systems, stable allelic variants can be distinguished. Irrespective of their nature, all such alleles have an underlying similarity: each is a bimodular hereditary unit, whose features depend on (i) a certain epigenetic mark (epigenetic determinant) in the DNA sequence or its product, and (ii) the DNA sequence itself (DNA determinant; if this is absent, the epigenetic allele fails to perpetuate). Thus, stable allelic epigenetic inheritance (SAEI) does not contradict the hereditary role of DNA, but involves additional molecular mechanisms with no or almost no limitations to their variety.

AB - Although epigenetic inheritance (EI) is a rapidly growing field of modern biology, it still has no clear place in fundamental genetic concepts which are traditionally based on the hereditary role of DNA. Moreover, not all mechanisms of EI attract the same attention, with most studies focused on DNA methylation, histone modification, RNA interference and amyloid prionization, but relatively few considering other mechanisms such as stable inhibition of plastid translation. Herein, we discuss all known and some hypothetical mechanisms that can underlie the stable inheritance of phenotypically distinct hereditary factors that lack differences in DNA sequence. These mechanisms include (i) regulation of transcription by DNA methylation, histone modifications, and transcription factors, (ii) RNA splicing, (iii) RNA-mediated post-transcriptional silencing, (iv) organellar translation, (v) protein processing by truncation, (vi) post-translational chemical modifications, (vii) protein folding, and (viii) homologous and non-homologous protein interactions. The breadth of this list suggests that any or almost any regulatory mechanism that participates in gene expression or gene-product functioning, under certain circumstances, may produce EI. Although the modes of EI are highly variable, in many epigenetic systems, stable allelic variants can be distinguished. Irrespective of their nature, all such alleles have an underlying similarity: each is a bimodular hereditary unit, whose features depend on (i) a certain epigenetic mark (epigenetic determinant) in the DNA sequence or its product, and (ii) the DNA sequence itself (DNA determinant; if this is absent, the epigenetic allele fails to perpetuate). Thus, stable allelic epigenetic inheritance (SAEI) does not contradict the hereditary role of DNA, but involves additional molecular mechanisms with no or almost no limitations to their variety.

KW - epigenetic inheritance

KW - DNA methylation

KW - histone modification

KW - chromatin remodelling

KW - bistable gene networks

KW - hereditary prions

KW - RNA interference

KW - self-splicing

KW - trans-generation memory

KW - body-to-body information transfer.

KW - epigenetic inheritance

KW - DNA methylation

KW - histone modification

KW - chromatin remodelling

KW - bistable gene networks

KW - hereditary prions

KW - RNA interference

KW - self-splicing

KW - trans-generation memory

KW - body-to-body information transfer.

KW - body-to-body information transfer

KW - DEOXYRIBONUCLEIC-ACID

KW - POLYPEPTIDE-CHAIN

KW - ARABIDOPSIS-THALIANA

KW - SMALL RNAS

KW - DNA METHYLATION

KW - PODOSPORA-ANSERINA

KW - GROUP-I INTRONS

KW - YEAST SACCHAROMYCES-CEREVISIAE

KW - GENE-EXPRESSION

KW - TRANSGENERATIONAL INHERITANCE

UR - http://www.scopus.com/inward/record.url?scp=85047498624&partnerID=8YFLogxK

UR - http://www.mendeley.com/research/mechanisms-epigenetic-inheritance-diverse

U2 - doi: 10.1111/brv.12429

DO - doi: 10.1111/brv.12429

M3 - Article

VL - 93

SP - 1987

EP - 2005

JO - Biological Reviews

JF - Biological Reviews

SN - 1464-7931

IS - 4

ER -

ID: 35735217