DNA Methyltransferases and Structural-Functional Specificity of Eukaryotic DNA Modification

Buryanov, Yа. I.; Шевчук, Т. В.

doi:10.1007/s10541-005-0178-0

Cited by 31 publications

(20 citation statements)

References 157 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Studies with postmortem brain samples from schizophrenic patients reveal increased DNA methylation of the GAD1 promoter Grayson et al, 2006;Kundakovic et al, 2007). DNA methylation associates with gene silencing and cortical GABAergic neurons from schizophrenic patients also show increased expression of DNA methyltransferase 1 , which catalyzes cytosine methylation (Buryanov and Shevchuk, 2005;Goll and Bestor, 2005). Decreased GAD1 transcription is linked to increased DNMT1 association with the GAD1 promoter (Kundakovic et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Maternal Care and DNA Methylation of a Glutamic Acid Decarboxylase 1 Promoter in Rat Hippocampus

Zhang¹,

Hellstrom²,

Bagot³

et al. 2010

J. Neurosci.

251

170

View full text Add to dashboard Cite

Parenting and the early environment influence the risk for various psychopathologies. Studies in the rat suggest that variations in maternal care stably influence DNA methylation, gene expression, and neural function in the offspring. Maternal care affects neural development, including the GABAergic system, the function of which is linked to the pathophysiology of diseases including schizophrenia and depression. Postmortem studies of human schizophrenic brains have revealed decreased forebrain expression of glutamic acid decarboxylase 1 (GAD1) accompanied by increased methylation of a GAD1 promoter. We examined whether maternal care affects GAD1 promoter methylation in the hippocampus of adult male offspring of high and low pup licking/grooming (high-LG and low-LG) mothers. Compared with the offspring of low-LG mothers, those reared by high-LG dams showed enhanced hippocampal GAD1 mRNA expression, decreased cytosine methylation, and increased histone 3-lysine 9 acetylation (H3K9ac) of the GAD1 promoter. DNA methyltransferase 1 expression was significantly higher in the offspring of low-compared with high-LG mothers. Pup LG increases hippocampal serotonin (5-HT) and nerve growth factor-inducible factor A (NGFI-A) expression. Chromatin immunoprecipitation assays revealed enhanced NGFI-A association with and H3K9ac of the GAD1 promoter in the hippocampus of high-LG pups after a nursing bout. Treatment of hippocampal neuronal cultures with either 5-HT or an NGFI-A expression plasmid significantly increased GAD1 mRNA levels. The effect of 5-HT was blocked by a short interfering RNA targeting NGFI-A. These results suggest that maternal care influences the development of the GABA system by altering GAD1 promoter methylation levels through the maternally induced activation of NGFI-A and its association with the GAD1 promoter.

show abstract

Section: Introductionmentioning

confidence: 99%

Maternal Care and DNA Methylation of a Glutamic Acid Decarboxylase 1 Promoter in Rat Hippocampus

Zhang¹,

Hellstrom²,

Bagot³

et al. 2010

J. Neurosci.

251

170

View full text Add to dashboard Cite

show abstract

“…This stands in stark contrast to methylation at CG sites which is correlated with a variety of clastic events including viral integration, genetic recombination, gene expansion, as well as transcriptional silencing. [2][3][4][5][6][7][8][9] Consistent with this contrast are the findings 10 that the expression of the bacterial G M CGC methyltransferase M•HhaI resulted in increased numbers of soft agar foci, formed by Mouse 3T3 cells, while the expression of the bacterial C M CWGG methyltransferase M•EcoRII had no detectable biological effect 11 on human HK293 cells.…”

Section: Introductionmentioning

confidence: 84%

Distribution of CWG and CCWGG in the Human Genome

Watson

Munson²,

Clark³

et al. 2007

Epigenetics

View full text Add to dashboard Cite

Expression of the bacterial CG methyltransferase M•HhaI in mammalian cells appears to generate significant biological effects, while biological effects of the expression of the non-CG methyltransferase M•EcoRII in human cells have not been detected. The association of cytosine methylation with the CG site in mammals is also associated with clustering of CG sites near 5' control regions (CG-islands) of human genes. Moreover spontaneous deamination of 5-methylcytosine at these sites is thought to lead to the well known deficiency of CG sites in genomes where endogenous CG methyltransferases are expressed. Since these associations are generally taken to imply a biological function for the CG dinucleotide that is associated with its selective methylation by endogenous DNA methylation systems, we have asked whether or not CWG or CCWGG sites are clustered in regions flanking human genes and whether or not an overall deficiency of CWG or CCWGG occurs in the human genome. Using build 36.1, of the human genome, we inspected the regions flanking the 28,501 well known gene loci in the human genome. Our analysis confirmed the expected clustering of CG sites near the 5' region of known genes and open reading frames. In contrast to the CG site, neither the CWG site nor the CCWGG site recognized by the bacterial methyltransferase M•EcoRII were clustered in any particular region near known genes and open reading frames. Moreover, neither the CCWGG nor the CWG site was depleted in the human genome, again in sharp contrast to the known genomic deficiency of CpG sites. Our findings suggest that in contrast to CG site recognition, human cytosine methyltransferases recognize CWG and CCWGG only at very low frequency if at all.

show abstract

“…The role of DNMT1 is to preserve the DNA methylation pattern after DNA replication during mitotic cell division as well as after fertilization [46], a process guided by the presence of hemi-methylated CpGs, which are recognized by DNMT1 in dsDNA [47]. Additionally, DNMT3a and DNMT3b catalyze de novo methylation allowing the establishment of new DNA methylation patterns during gametogenesis, embryonic development, and cell differentiation [46,48].…”

Section: Dna Methylationmentioning

confidence: 99%

Epigenetic Programming of Cardiovascular Disease by Perinatal Hypoxia and Fetal Growth Restriction

Casanello¹,

Herrera²,

Krause³

2017

Hypoxia and Human Diseases

View full text Add to dashboard Cite

Most of the worldwide deaths in patients with non-communicable diseases are due to cardiovascular and metabolic diseases, which are determined by a mix of environmental, genetic and epigenetic factors, and by their interactions. The aetiology of most cardiovascular diseases has been partially linked with in utero adverse conditions that may increase the risk of developing diseases later in life, known as Developmental Origins of Health and Disease (DOHaD). Perinatal hypoxia can program the fetal and postnatal developmental patterns, resulting in permanent modifications of cells, organs and systems function. In spite of the vast evidence obtained from human and animal studies linking development under adverse intrauterine conditions with increased cardiovascular risk, still few is known about the specific effects of intrauterine oxygen deficiency and the related pathogenic mechanisms. Currently, the most accepted processes that program cellular function are epigenetic mechanisms which determine gene expression in a cell-specific fashion. In this chapter we will review the current literature regarding the perinatal exposure to chronic hypoxia and Fetal Growth Restriction (FGR) in humans and animals and how this impinges the cardiovascular physiology through epigenetic, biochemical, morphologic and pathophysiologic modifications that translate into diseases blasting at postnatal life.

show abstract

DNA Methyltransferases and Structural-Functional Specificity of Eukaryotic DNA Modification

Cited by 31 publications

References 157 publications

Maternal Care and DNA Methylation of a Glutamic Acid Decarboxylase 1 Promoter in Rat Hippocampus

Maternal Care and DNA Methylation of a Glutamic Acid Decarboxylase 1 Promoter in Rat Hippocampus

Distribution of CWG and CCWGG in the Human Genome

Epigenetic Programming of Cardiovascular Disease by Perinatal Hypoxia and Fetal Growth Restriction

Contact Info

Product

Resources

About