Growth regulation of mouse DNA methyltransferase gene expression

Szyf, Moshe; Bozovic, V; Tanigawa, G

doi:10.1016/s0021-9258(18)99179-9

Cited by 120 publications

(10 citation statements)

References 34 publications

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“…This covalent modification of DNA is catalyzed by DNA (cytosine-5 0 ) methyltransferases (DNMTs) and involves the transfer of a methyl group to the 5 0 position of cytosine residues, canonically at CG dinucleotides. Expression and activity of DNMTs is generally restricted to dividing cells and is very high during early development (Szyf et al, 1985(Szyf et al, , 1991Monk et al, 1987;Singer-Sam et al, 1990;Goto et al, 1994). DNA methylation can induce long-term transcriptional silencing through direct interference with transcription factor binding.…”

Section: Introductionmentioning

confidence: 99%

“…DNA methylation has been studied extensively in development and has long been considered a static process following cell differentiation, because typically DNMT expression greatly diminishes once terminal differentiation has occurred (Bestor et al, 1988;Szyf et al, 1985Szyf et al, , 1991Monk et al, 1987;Singer-Sam et al, 1990;Goto et al, 1994;Deng and Szyf, 1999). Because the mammalian brain primarily consists of postmitotic neurons and glial cells that possess relatively low proliferative potential, reports that the adult mammalian CNS possesses high levels of DNMT mRNA and enzymatic activity were unexpected (Monk et al, 1987;Goto et al, 1994;Brooks et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

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Covalent Modification of DNA Regulates Memory Formation

Miller

Sweatt

2007

Neuron

1,097

1,094

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DNA methylation is a covalent chemical modification of DNA catalyzed by DNA methyltransferases (DNMTs). DNA methylation is associated with transcriptional silencing and has been studied extensively as a lifelong molecular information storage mechanism put in place during development. Here we report that DNMT gene expression is upregulated in the adult rat hippocampus following contextual fear conditioning and that DNMT inhibition blocks memory formation. In addition, fear conditioning is associated with rapid methylation and transcriptional silencing of the memory suppressor gene PP1 and demethylation and transcriptional activation of the synaptic plasticity gene reelin, indicating both methyltransferase and demethylase activity during consolidation. DNMT inhibition prevents the PP1 methylation increase, resulting in aberrant transcription of the gene during the memory-consolidation period. These results demonstrate that DNA methylation is dynamically regulated in the adult nervous system and that this cellular mechanism is a crucial step in memory formation.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Covalent Modification of DNA Regulates Memory Formation

Miller

Sweatt

2007

Neuron

1,097

1,094

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“…This direct interplay of MeCP2-DNMT1 complex was suggested to be responsible for genome-wide DNA methylation [ 53 ]. The expression of DNMT1 was induced as DNA synthesis complete in proliferating cells [ 54 ], which may also induce the expression of MeCP2. This might explain the cause of increase in MeCP2 expression in the control group with or without MT treatment in this study.…”

Section: Discussionmentioning

confidence: 99%

Melatonin-induced suppression of DNA methylation promotes odontogenic differentiation in human dental pulp cells

Deng

Fan

et al. 2020

Bioengineered

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Differentiation potency of human dental pulp cells (hDPCs) is essential for dentin regeneration. DNA methylation is one of the major epigenetic mechanisms and is suggested to involve in differentiation of hDPCs, the machinery of which includes DNA methyltransferase enzymes (DNMTs) and methyl-CpG-binding domain proteins (MBDs). Our previous study has found that melatonin (MT) promoted hDPC differentiation, but its mechanism remains elusive. We aimed to investigate the role of DNA methylation in the promotion of MT to differentiation of hDPCs in vitro . hDPCs were cultured in basal growth medium (CO) or odontogenic medium (OM) exposed to MT at different concentrations (0, 10 −12 , 10 −10 , 10 −8 , 10 −6 , 10 −4 M). The cell growth was analyzed using Cell Counting Kit-8 assay, and mineralized tissue formation was measured using Alizarin red staining. The expression of the 10 genes ( DNMT1, DNMT3A, DNMT3B, MBD1-6, MeCP2 ) was determined using real-time qPCR and western blotting. The abundance of MeCP2 in the nuclei was evaluated using immunofluorescence analysis. Global methylation level was tested using ELISA. We found that mineralized tissue formation significantly increased in OM with MT at 10 −4 M, while the levels of MeCP2 and global DNA methylation level declined. The expression of MBD1, MBD3, and MBD4 significantly increased in OM alone, and the expession of DNMT1 and MBD2 was decreased. These results indicate that MT promotes odontogenic differentiation of hDPCs in vitro by regulating the levels of DNMT1, MeCP2, and global DNA methylation, suggesting that MT-induced DNA methylation machinery may play an important role in tooth regeneration.

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“…DNMT1 is known as the maintenance methyltransferase as it has a higher preference for hemimethylated CpG dinucleotides [90,91]. Moreover, DNMT1 expression is high during the S phase of the cell cycle when DNA is replicated, supporting its posited role in replicating the methylation pattern onto the daughter strand from the hemimethylated DNA [92,93]. The DNMT3 family is known for its role in de novo methylation.…”

Section: (B) Dna Methylationmentioning

confidence: 99%

Looking beyond the DNA sequence: the relevance of DNA methylation processes for the stress–diathesis model of depression

Booij

Wang

Lévesque

et al. 2013

Phil. Trans. R. Soc. B

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The functioning of the hypothalamic–pituitary–adrenal (HPA) axis and serotonergic (5-HT) system are known to be intertwined with mood. Alterations in these systems are often associated with depression. However, neither are sufficient to cause depression in and of themselves. It is now becoming increasingly clear that the environment plays a crucial role, particularly, the perinatal environment. In this review, we posit that early environmental stress triggers a series of epigenetic mechanisms that adapt the genome and programme the HPA axis and 5-HT system for survival in a harsh environment. We focus on DNA methylation as it is the most stable epigenetic mark. Given that DNA methylation patterns are in large part set within the perinatal period, long-term gene expression programming by DNA methylation is especially vulnerable to environmental insults during this period. We discuss specific examples of genes in the 5-HT system (serotonin transporter) and HPA axis (glucocorticoid receptor and arginine vasopressin enhancer) whose DNA methylation state is associated with early life experience and may potentially lead to depression vulnerability. We conclude with a discussion on the relevance of studying epigenetic mechanisms in peripheral tissue as a proxy for those occurring in the human brain and suggest avenues for future research.

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Growth regulation of mouse DNA methyltransferase gene expression

Cited by 120 publications

References 34 publications

Covalent Modification of DNA Regulates Memory Formation

Covalent Modification of DNA Regulates Memory Formation

Melatonin-induced suppression of DNA methylation promotes odontogenic differentiation in human dental pulp cells

Looking beyond the DNA sequence: the relevance of DNA methylation processes for the stress–diathesis model of depression

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