Cooperative interactions between epigenetic modifications and their function in the regulation of chromosome architecture

Weissmann, Frank; Lyko, Frank

doi:10.1002/bies.10314

Cited by 23 publications

(15 citation statements)

References 62 publications

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“…Modification of gene expression through alteration of chromatin structure has been found in many eukaryotic organisms, including nematodes (Ryner & Swain, 1995;Kelly & Fire, 1998), Drosophila (Weissmann & Lyko, 2003), plants (van Blokland et al, 1997), mammals (Bird & Wolffe, 1999), yeasts and fungi (Roth, 1995;Selker, 1998).…”

Section: Discussionmentioning

confidence: 99%

Internuclear gene silencing in Phytophthora infestans is established through chromatin remodelling

et al. 2008

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In the plant pathogen Phytophthora infestans, nuclear integration of inf1 transgenic DNA sequences results in internuclear gene silencing of inf1. Although silencing is regulated at the transcriptional level, it also affects transcription from other nuclei within heterokaryotic cells of the mycelium. Here we report experiments exploring the mechanism of internuclear gene silencing in P. infestans. The DNA methylation inhibitor 5-azacytidine induced reversion of the inf1-silenced state. Also, the histone deacetylase inhibitor trichostatin-A was able to reverse inf1 silencing. inf1-expression levels returned to the silenced state when the inhibitors were removed except in non-transgenic inf1-silenced strains that were generated via internuclear gene silencing, where inf1 expression was restored permanently. Therefore, inf1-transgenic sequences are required to maintain the silenced state. Prolonged culture of non-transgenic inf1-silenced strains resulted in gradual reactivation of inf1 gene expression. Nuclease digestion of inf1-silenced and nonsilenced nuclei showed that inf1 sequences in silenced nuclei were less rapidly degraded than non-silenced inf1 sequences. Bisulfite sequencing of the endogenous inf1 locus did not result in detection of any cytosine methylation. Our findings suggest that the inf1-silenced state is based on chromatin remodelling. INTRODUCTIONIn many organisms, including animals, plants, fungi and protists, transcriptional gene silencing (TGS) can occur as a consequence of the introduction of transgenes into the somatic genome (Selker, 1997;Henikoff, 1998;Vaucheret et al., 1998;Cogoni & Macino, 1999;van West et al., 1999). TGS is thought to have evolved as a mechanism to protect the nuclear genome against potentially harmful transforming sequences such as transposons and viruses (Kooter et al., 1999). TGS is reminiscent of paramutation found in plants, and other imprinting phenomena (Hollick et al., 1997). Paramutation is an epigenetic phenomenon in which one allele or locus spontaneously acquires a less transcriptionally active state, which is then imposed on homologous sequences in the genome (Chandler et al., 2000). In plants and animals TGS is often, but not invariably associated with altered methylation patterns and changes in chromatin structure. Organisms lacking efficient DNA methylation systems, such as Drosophila, Caenorhabditis elegans and yeast, use chromatin modification to achieve imprinting and to maintain epigenetic states. Several experiments have shown that chromatin remodelling and histone deacetylation processes influence higher-order chromatin structure and can result in transcriptional repression (Tyler & Kadonaga, 1999;Grewal & Elgin, 2002;Vermaak et al., 2003).Other homology-dependent gene-silencing phenomena are also found; these are thought to occur at a posttranscriptional level in the cytoplasm. Post-transcriptional gene silencing (PTGS) phenomena have one major feature in common, which is that target mRNAs are degraded in a sequence-specific manner. Examples inclu...

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Section: Discussionmentioning

confidence: 99%

Internuclear gene silencing in Phytophthora infestans is established through chromatin remodelling

et al. 2008

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“…125,126 Although there are seemingly distinct roles for each of these mechanisms acting individually, we more often observe redundant and cooperative functions for which several mechanisms must work together for normal cellular function and development. 127,128 Likewise, multiple mechanisms are simultaneously perturbed in disease states.…”

Section: Epigeneticsmentioning

confidence: 99%

Nutrigenomics, the Microbiome, and Gene-Environment Interactions: New Directions in Cardiovascular Disease Research, Prevention, and Treatment

Ferguson¹,

Allayee²,

Gerszten³

et al. 2016

Circ Cardiovasc Genet

101

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Abstract-Cardiometabolic diseases are the leading cause of death worldwide and are strongly linked to both genetic and nutritional factors. The field of nutrigenomics encompasses multiple approaches aimed at understanding the effects of diet on health or disease development, including nutrigenetic studies investigating the relationship between genetic variants and diet in modulating cardiometabolic risk, as well as the effects of dietary components on multiple "omic" measures, including transcriptomics, metabolomics, proteomics, lipidomics, epigenetic modifications, and the microbiome. Here, we describe the current state of the field of nutrigenomics with respect to cardiometabolic disease research and outline a direction for the integration of multiple omics techniques in future nutrigenomic studies aimed at understanding mechanisms and developing new therapeutic options for cardiometabolic disease treatment and prevention. The interpretation and scope of nutrigenomics may vary, but it can be thought to encompass the spectrum of nutritional genomics research, including classic nutrigenetics studies of gene-diet interactions and molecular nutrition, in vitro and in vivo models, human nutrition studies, and the application of largescale, unbiased studies using high-throughput "omics" techniques to study the effects of nutrients on the body. 6 As the Figure shows, diet and the genome may influence cardiometabolic health through a variety of interconnected intermediates, perturbations in which can be measured through omics technologies, including RNA expression (transcriptome), epigenetic modifications (epigenome), metabolites (metabolome), lipids (lipidome), proteins (proteome), and resident microbial communities (microbiome). Although it is clear that both nutrients and genes play a distinct role in determining health, the complex interactions among genes, diet, and downstream networks are not well understood. The application of nutrigenomics approaches to questions of human health and disease is an important component in understanding the complexities of the interplay between basic metabolic processes and externalThe American Heart Association makes every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outside relationship or a personal, professional, or business interest of a member of the writing panel. Specifically, all members of the writing group are required to complete and submit a Disclosure Questionnaire showing all such relationships that might be perceived as real or potential conflicts of interest.This statement was approved by the American Heart Association Science Advisory and Coordinating Committee on January 22, 2016, and the American Heart Association Executive Committee on February 23, 2016. A copy of the document is available at http://professional.heart.org/statements by using either "Search for Guidelines & Statements" or the "Browse by Topic" area. To purchase additional reprints, call 843-216-2533 or e-mail kelle.ramsay@ wolterskluwer.com.The...

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“…One of the best-characterized PTMs is the acetylation of lysine 9 on H3 histone tails (H3K9ac), which is typically associated with an open chromatin state conducive to active gene transcription. [3][4][5][6] In contrast, methylation of lysine and/or arginine residues can be associated with either active or repressed gene states with histone H3K4 methylation primarily associated with active genes and H3K9 methylation correlating with gene repression. 7 An additional layer of complexity in the histone code is that methylation can exist in mono-, di-or trimethylated forms, which have distinct…”

Section: Introductionmentioning

confidence: 99%

The endoglycosidase heparanase enters the nucleus of T lymphocytes and modulates H3 methylation at actively transcribed genes via the interplay with key chromatin modifying enzymes

Sutcliffe

Bunting

et al. 2012

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Cooperative interactions between epigenetic modifications and their function in the regulation of chromosome architecture

Cited by 23 publications

References 62 publications

Internuclear gene silencing in Phytophthora infestans is established through chromatin remodelling

Internuclear gene silencing in Phytophthora infestans is established through chromatin remodelling

Nutrigenomics, the Microbiome, and Gene-Environment Interactions: New Directions in Cardiovascular Disease Research, Prevention, and Treatment

The endoglycosidase heparanase enters the nucleus of T lymphocytes and modulates H3 methylation at actively transcribed genes via the interplay with key chromatin modifying enzymes

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