Epigenetic Control of Gene Expression

Razin, Aharon; Shemer, Ruth

doi:10.1007/978-3-540-69111-2_9

Cited by 29 publications

(11 citation statements)

References 80 publications

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“…Global DNA hypomethylation plays an important role in many chemical carcinogenesis [45][46][47][48]. Methylation changes occur during oncogenic transformation with inorganic carcinogens such as arsenic, nickel, and Cd [10,[49][50].…”

Section: Global Dna Methylationmentioning

confidence: 99%

Cadmium and Its Epigenetic Effects

Wang

Shao³

et al. 2012

CMC

140

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Cadmium (Cd) is a toxic, nonessential transition metal and contributes a health risk to humans, including various cancers and cardiovascular diseases; however, underlying molecular mechanisms remain largely unknown. Cells transmit information to the next generation via two distinct ways: genetic and epigenetic. Chemical modifications to DNA or histone that alters the structure of chromatin without change of DNA nucleotide sequence are known as epigenetics. These heritable epigenetic changes include DNA methylation, post-translational modifications of histone tails (acetylation, methylation, phosphorylation, etc), and higher order packaging of DNA around nucleosomes. Apart from DNA methyltransferases, histone modification enzymes such as histone acetyltransferase, histone deacetylase, and methyltransferase, and microRNAs (miRNAs) all involve in these epigenetic changes. Recent studies indicate that Cd is able to induce various epigenetic changes in plant and mammalian cells in vitro and in vivo. Since aberrant epigenetics plays a critical role in the development of various cancers and chronic diseases, Cd may cause the above-mentioned pathogenic risks via epigenetic mechanisms. Here we review the in vitro and in vivo evidence of epigenetic effects of Cd. The available findings indicate that epigenetics occurred in association with Cd induction of malignant transformation of cells and pathological proliferation of tissues, suggesting that epigenetic effects may play a role in Cd toxic, particularly carcinogenic effects. The future of environmental epigenomic research on Cd should include the role of epigenetics in determining long-term and late-onset health effects following Cd exposure.

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Section: Global Dna Methylationmentioning

confidence: 99%

Cadmium and Its Epigenetic Effects

Wang

Shao³

et al. 2012

CMC

140

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“…DNA methylation is an enzymatic reaction performed by several types of DNAmethyltransferases [reviewed in Bestor, 2000]. A large number of genes exhibit an inverse correlation between the degree of methylation and gene expression, and there is an increasing body of experimental evidence suggesting that epiG modification is intimately involved in the regulation of expression of genes [Holliday, 1996;Holliday et al, 1996;Razin and Shemer, 1999;Yeivin and Razin, 1993]. One of the mechanisms of epiG regulation of genes is related to methylation of the binding sites for transcription factors that changes the affinity of such factors to regulatory sequences of specific genes [Riggs and Porter, 1996;Riggs et al, 1998].…”

Section: Basic Principles Of Epig Regulationmentioning

confidence: 99%

Epigenetics and bipolar disorder: New opportunities and challenges

Petronis

2003

American J of Med Genetics Pt C

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Despite significant effort, understanding of the molecular causes and mechanisms of bipolar disorder (BD) remains a major challenge. Numerous molecular genetic linkage and association studies have been conducted over the last two decades; however, the data are quite inconsistent or even controversial. This article develops an argument that molecular studies of BD would benefit significantly from adding an epigenetic (epiG) perspective. EpiG factors refer to modifications of DNA and chromatin that "orchestrate" the activity of the genome, including regulation of gene expression. EpiG mechanisms are consistent with various non-Mendelian features of BD such as the relatively high degree of discordance in monozygotic (MZ) twins, the critical age group for susceptibility to the disease, clinical differences in males and females, and fluctuation of the disease course, including interchanges of manic and depressive phases, among others. Apart from the phenomenological consistency, molecular epiG peculiarities may shed new light on the understanding of controversial molecular genetic findings. The relevance of epigenetics for the molecular studies of BD is demonstrated using the examples of genetic studies of BD on chromosome 11p and the X chromosome. A spectrum of epiG mechanisms such as genomic imprinting, tissue-specific effects, paramutagenesis, and epiG polymorphism, as well as epiG regulation of X chromosome inactivation, is introduced. All this serves the goal of demonstrating that epiG factors cannot be ignored anymore in complex phenotypes such as BD, and systematic large-scale epiG studies of BD have to be initiated.

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“…60 The DMR signals need to be translated by MBD proteins. Therefore, the hypothesis that imprinting patterns might not be established or maintained normally in the absence of MeCP2 has been tested in RTT cell lines and tissue samples.…”

Section: Downstream Effects Of Mecp2 Deficiency No Loss Of Gene Imprimentioning

confidence: 99%

Mechanisms of Disease: neurogenetics of MeCP2 deficiency

Francke

2006

Nat Rev Neurol

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Rett syndrome (RTT) is unique among genetic, chromosomal and other developmental disorders because of its extreme female gender bias, early normal development, and subsequent developmental regression with loss of motor and language skills. RTT is caused by heterozygosity for mutations in the X-linked gene MECP2, which encodes methyl-CpG binding protein 2. MeCP2 is a multifunctional protein that can act as an architectural chromatin-binding protein, a function that is unrelated to its ability to bind methyl-CpG and to attract chromatin modification complexes. Inactivating mutations that cause RTT in females are not prenatally lethal in males, but lead to profound congenital encephalopathy. Molecular diagnoses of RTT, through demonstration of a MECP2 mutation, made at an early stage of the disorder, usually confirm the sporadic nature and very low recurrence risk of the condition. A positive DNA test result, however, also predicts the inevitable clinical course, given the lack of effective intervention. Initial hypotheses indicating that the MeCP2 protein acts as a genome-wide transcriptional repressor were not confirmed by global gene expression studies in various tissues of individuals with RTT and mouse models of MeCP2 deficiency. Rather, recent evidence points to low-magnitude effects of a small number of genes--including the brain--derived neurotrophic factor pathway and glucocorticoid response genes-that might affect formation and maturation of synapses or synaptic function in postmitotic neurons.

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Epigenetic Control of Gene Expression

Cited by 29 publications

References 80 publications

Cadmium and Its Epigenetic Effects

Cadmium and Its Epigenetic Effects

Epigenetics and bipolar disorder: New opportunities and challenges

Mechanisms of Disease: neurogenetics of MeCP2 deficiency

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