Regulation of imprinting: A multi‐tiered process

Rand, Eyal; Cedar, Howard

doi:10.1002/jcb.10352

Cited by 26 publications

(19 citation statements)

References 38 publications

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“…Noncoding, functional RNAs have been shown to be involved in genomic imprinting (8) and X inactivation. (6) However, a farmore-widespread phenomenon, RNA interference (RNAi) is emerging as an essential mechanism in the establishment of eukaryotic heterochromatin from yeast to mammals (14,15) (Figs.…”

Section: Noncoding Functional Rnamentioning

confidence: 99%

“…In Drosophila and mammals, PcG proteins work together in promoter-binding complexes, which may contain a SET domain HMT and/or a histone-binding Polycomb homologue. (7,8) These proteins in turn bind to corepressors, HDACs, chromatin-remodelling proteins and RNA. (7,43,44) For example, the human PcG HMT EZH2 methylates H3-K27 and binds Polycomb homologue HPC2 (Fig.…”

Section: Hp1 and Polycombmentioning

confidence: 99%

“…(5,48) DNMT3B is responsible for de novo methylation and the structural integrity of pericentric DNA, and for methylation of imprinting centres and CpG islands on the Xi. (8,49) …”

Section: Hp1 and Polycombmentioning

confidence: 99%

“…(56,57) In addition, MeCP2 was shown to tether histone methylation activity to a methylated transgene (55) and methylation of imprinting centres can trigger heterochromatin formation. (8,48) Our knowledge of the mechanisms behind this is sketchy, but we do know that some proteins can bind specifically to unmethylated imprinting centres to prevent subsequent CpG methylation. (56) In cancer, de novo CpG methylation accompanies gene silencing and precedes histone methylation.…”

Section: Methyl Cpg-binding Proteins (Mecps)mentioning

confidence: 99%

“…(6) Facultative heterochromatin can also encompass the promotors of genes silenced during development. (7,8) This type of heterochromatin has previously been referred to as ''silent chromatin'', (3) ''intercalary'' heterochromatin (9) or heterochromatin-like. (7) In addition, most neocentromeres (centromeres arising de novo from ectopic locations) switch from a euchromatic to a heterochromatic state.…”

Section: Introductionmentioning

confidence: 99%

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Heterochromatin?many flavours, common themes

Craig

2004

Bioessays

115

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SummaryHeterochromatin remains condensed throughout the cell cycle, is generally transcriptionally inert and is built and maintained by groups of factors with each group member sharing a similar function. In mammals, these groups include sequence-specific transcriptional repressors, functional RNA and proteins involved in DNA and histone methylation. Heterochromatin is cemented together via interactions within and between each protein group and is maintained by the cell's replication machinery. It can be constitutive (permanent) or facultative (developmentally regulated) and be any size, from a gene promotor to a whole genome. By studying the formation of facultative heterochromatin, we have gained information about how heterochromatin is assembled. We have discovered that there are many different architectural plans for the building of heterochromatin, leading to a seemingly never-ending variety of heterochromatic loci, with each built according to a general rule.

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Section: Noncoding Functional Rnamentioning

confidence: 99%

Section: Hp1 and Polycombmentioning

confidence: 99%

“…(5,48) DNMT3B is responsible for de novo methylation and the structural integrity of pericentric DNA, and for methylation of imprinting centres and CpG islands on the Xi. (8,49) …”

Section: Hp1 and Polycombmentioning

confidence: 99%

Section: Methyl Cpg-binding Proteins (Mecps)mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Heterochromatin?many flavours, common themes

Craig

2004

Bioessays

115

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Five azacytidine, a DNA methyltransferase inhibitor, specifically inhibits testicular cord formation and Sertoli cell differentiation in vitro

Mizukami

Kanai

Fujisawa

et al. 2007

Molecular Reproduction Devel

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In mammals, Sry, Sox9, and M33 act as regulators at a chromatin level and promote the maturation of embryonic gonads into testes. Recently, it was shown that transcriptional regulation by DNA methylation plays crucial roles in gene expression during the differentiation and development of various cell types. To determine the involvement of DNA methylation in sex determination of the gonad, we developed and performed organ culture of gonad with the DNA methyltransferase inhibitor 5-azacytidine to induce global DNA methylation status changes. In vitro treatment with 5-azacytidine specifically inhibited testicular cord formation in a dose-dependent manner; however, no appreciable defect was observed in ovarian explants. Inhibition of testicular cord was observed only in gonads from 11.5 days post-coitus embryos. These effects were not observed in 5-azacytidine-treated gonads from 12.0 days post-coitus embryos. To determine the effect of 5-azacytidine on Sertoli and Leydig cell differentiation in the testis, we performed whole mount in situ hybridization analysis. The Leydig and stromal cell marker genes Lhx9, Mfge8, and 3beta-Hsd were normally induced in 5-azaytidine-treated testicular explants. Sertoli cell marker genes, Sox9 and MIS were normally induced, but Col9a3, encoding an extracellular matrix component, was inhibited in 5-azacytidine-treated testicular explants. Thus, our data show that DNA methylation is involved in testicular cord formation and Sertoli cell differentiation, acting directly on the gonad at 11.5 days post-coitus.

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Reduced salivary gland size and increased presence of epithelial progenitor cells in DLK1-deficient mice

et al. 2015

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DLK1 (PREF1, pG2, or FA1) is a transmembrane and secreted protein containing epidermal growth factor-like repeats. Dlk1 expression is abundant in many tissues during embryonic and fetal development and is believed to play an important role in the regulation of tissue differentiation and fetal growth. After birth, Dlk1 expression is abolished in most tissues but is possibly reactivated to regulate stem cell activation and responses to injury. We have recently reported that DLK1 regulates many aspects of salivary gland organogenesis. Here, we have extended our studies of the salivary gland phenotype of Dlk1 knock-out mice. We have observed that salivary glands are smaller and weigh significantly less in both Dlk1 knock-out males and females compared with gender and age-matched wild-type mice and regardless of the natural sexual dimorphism in rodent salivary glands. This reduced size correlates with a reduced capacity of Dlk1-deficient mice to secrete saliva after stimulation with pilocarpine. However, histological and ultrastructural analyses of both adult and developing salivary gland tissues have revealed no defects in Dlk1 ((-/-)) mice, indicating that genetic compensation accounts for the relatively mild salivary phenotype in these animals. Finally, despite their lack of severe anomalies, we have found that salivary glands from Dlk1-deficient mice present a higher amount of CK14-positive epithelial progenitors at various developmental stages, suggesting a role for DLK1 in the regulation of salivary epithelial stem cell balance.

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Regulation of imprinting: A multi‐tiered process

Cited by 26 publications

References 38 publications

Heterochromatin?many flavours, common themes

Heterochromatin?many flavours, common themes

Five azacytidine, a DNA methyltransferase inhibitor, specifically inhibits testicular cord formation and Sertoli cell differentiation in vitro

Reduced salivary gland size and increased presence of epithelial progenitor cells in DLK1-deficient mice

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