High Histone Acetylation and Decreased Polycomb Repressive Complex 2 Member Levels Regulate Gene Specific Transcriptional Changes During Early Embryonic Stem Cell Differentiation Induced by Retinoic Acid

Lee, Elliot R; Murdoch, Fern E.; Fritsch, Michael K.

doi:10.1634/stemcells.2007-0203

Cited by 73 publications

(53 citation statements)

References 71 publications

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“…These results indicate that PINK1 influences H3-K27 trimethylation during neuronal differentiation triggered by RA. Several neuronal differentiation genes, such as Neurogenin 2 (NeuroG2) or Nestin (Nes) (22,44), are targets of PRC2. To evaluate if PINK1 may affect the SH-SY5Y cell differentiation program through regulation of PRC2 function, we quantified by reverse-transcriptionquantitative PCR (RT-qPCR) the expression of the aforementioned PRC2-target genes on PINK1 stably overexpressing or PINK1-silenced SH-SY5Y cells treated with RA.…”

Section: Pink1 Modulates the Differentiation Gene-expression Pattern mentioning

confidence: 99%

RETRACTED: PINK1 regulates histone H3 trimethylation and gene expression by interaction with the polycomb protein EED/WAIT1

Berthier

Jiménez-Sáinz

Pulido

2013

Proc. Natl. Acad. Sci. U.S.A.

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Mutations in PTEN-induced putative kinase 1 (PINK1) gene are associated to early-onset recessive forms of Parkinson disease. PINK1 function is related to mitochondria homeostasis, but the molecular pathways in which PINK1 is involved are largely unknown. Here, we report the identification of the embryonic ectoderm development polycomb histone-methylation modulator (EED/WAIT1) as a PINK1-interacting and -regulated protein. The PINK1:EED/WAIT1 physical interaction was mediated by the PINK1 kinase domain and the EED/WAIT1 40 amino acid ending with tryptophan and aspartate (WD40)-repeat region, and PINK1 phosphorylated EED/WAIT1 in vitro. PINK1 associated with EED/WAIT1 in cells and relocated EED/WAIT1 to the mitochondria. This interaction reduced the trimethylation of lysine 27 from histone H3, which affected polycomb-regulated gene transcription during RA differentiation of SH-SY5Y human neuroblastoma cells. Our findings unveil a pathway by which PINK1 regulates histone methylation and gene expression through the polycomb repressor complex.

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Section: Pink1 Modulates the Differentiation Gene-expression Pattern mentioning

confidence: 99%

RETRACTED: PINK1 regulates histone H3 trimethylation and gene expression by interaction with the polycomb protein EED/WAIT1

Berthier

Jiménez-Sáinz

Pulido

2013

Proc. Natl. Acad. Sci. U.S.A.

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“…Global levels of Ezh2 and H3K27me3 decrease when mouse embryonic stem cells differentiate and PRC2 target genes specifically lose Ezh2 binding and H3K27me3 enrichment (28). In addition, two groups found that miR-101 was up-regulated after differentiation of human embryonic stem cell lines (29,30).…”

Section: Resultsmentioning

confidence: 99%

The Putative Tumor Suppressor microRNA-101 Modulates the Cancer Epigenome by Repressing the Polycomb Group Protein EZH2

Friedman

Liang

Liu³

et al. 2009

Cancer Research

363

257

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The Polycomb Repressive Complex 2 (PRC2) mediates epigenetic gene silencing by trimethylating histone H3 lysine 27 (H3K27me3) and is known to aberrantly silence tumor suppressor genes in cancer. EZH2, the catalytic subunit of PRC2, enhances tumorigenesis and is commonly overexpressed in several types of cancer. Our microRNA profiling of bladder transitional cell carcinoma (TCC) patient samples revealed that microRNA-101 (miR-101) is down-regulated in TCC, and we showed that miR-101 inhibits cell proliferation and colony formation in TCC cell lines. Furthermore, our results confirm that miR-101 directly represses EZH2 and stable EZH2 knockdowns in TCC cell lines create a similar growth suppressive phenotype. This suggests that abnormal down-regulation of miR-101 could lead to the overexpression of EZH2 frequently seen in cancer. We conclude that miR-101 may be a potent tumor suppressor by altering global chromatin structure through repression of EZH2. [Cancer Res 2009;69(6):2623-9]

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“…As a consequence of histone acetylation and decompacted chromatin structure, transcription factors and the basal transcriptional machinery are recruited to the region and activate gene transcription (50 -52). Previous study has shown that an increased acetylation of histones H3 and H4 by retinoic acid regulates gene specific transcriptional changes during early embryonic stem cell differentiation (53). ATRA and histone deacetylase inhibitor have been shown to increase Sp1 binding and acetylation of histones H3 and H4 in the promoter of folate receptor (54).…”

Section: Discussionmentioning

confidence: 98%

Interactive Roles of Ets-1, Sp1, and Acetylated Histones in the Retinoic Acid-dependent Activation of Guanylyl Cyclase/Atrial Natriuretic Peptide Receptor-A Gene Transcription

Kumar

Garg

Bolden

et al. 2010

Journal of Biological Chemistry

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Cardiac hormones atrial and brain natriuretic peptides activate guanylyl cyclase/natriuretic peptide receptor-A (GC-A/ NPRA), which plays a critical role in reduction of blood pressure and blood volume. Currently, the mechanisms responsible for regulating the Npr1 gene (coding for GC-A/NPRA) transcription are not well understood. The present study was conducted to examine the interactive roles of all-trans retinoic acid (ATRA), Ets-1, Sp1, and histone acetylation on the transcriptional regulation and function of the Npr1 gene. Deletion analysis of the Npr1 promoter and luciferase assays showed that ATRA enhanced a 16-fold Npr1 promoter activity and greatly stimulated guanylyl cyclase (GC) activity of the receptor protein in both atrial natriuretic peptide (ANP)-dependent and -independent manner. As confirmed by gel shift and chromatin immunoprecipitation assays, ATRA enhanced the binding of both Ets-1 and Sp1 to the Npr1 promoter. The retinoic acid receptor ␣ (RAR␣) was recruited by Ets-1 and Sp1 to form a transcriptional activator complex with their binding sites in the Npr1 promoter. Interestingly, ATRA also increased the acetylation of histones H3 and H4 and enhanced their recruitment to Ets-1 and Sp1 binding sites within the Npr1 promoter. Collectively, the present results demonstrate that ATRA regulates Npr1 gene transcription and GC activity of the receptor by involving the interactive actions of Ets-1, Sp1, and histone acetylation. Atrial natriuretic peptide (ANP)2 is a circulatory hormone, which plays a pivotal role in the regulation of sodium excretion, fluid volume, steroidogenesis, and cell proliferation, important factors in the control of blood pressure and blood volume (1-4). One of the principal loci involved in the regulatory actions of ANP is the guanylyl cyclase/natriuretic peptide receptor-A (GC-A/NPRA), which produces the intracellular second messenger cGMP, thus plays a central role in the pathophysiology of hypertension and cardiovascular disorders (4 -7). The signaling of ANP/cGMP through its downstream effector proteins, including cGMP-dependent protein kinases, phosphodiesterases, and cyclic nucleotide-gated ion channels, mediates the cellular effects of NPRA (4, 8). Gene-targeting and expression studies of Npr1 (coding for GC-A/NPRA) have identified the hallmark significance of this receptor in protecting against renal and cardiac pathophysiological conditions such as inhibiting the cardiac hypertrophic growth and fibrosis, extracellular matrix remodeling, and cell proliferation (9 -13). Earlier studies have demonstrated a significant association of Npr1 gene variants with hypertensive family history, left ventricular mass index, and left ventricular septal wall thickness in human essential hypertension (14, 15). It has also been shown that a longer thymine adenine repeat unit in spontaneously hypertensive rats regulates the transcription of the Npr1 gene, thus affecting diastolic blood pressure (16). Little is known about transcriptional regulation of the Npr1 gene, but the activity an...

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High Histone Acetylation and Decreased Polycomb Repressive Complex 2 Member Levels Regulate Gene Specific Transcriptional Changes During Early Embryonic Stem Cell Differentiation Induced by Retinoic Acid

Abstract: ABSTRACT

Cited by 73 publications

References 71 publications

RETRACTED: PINK1 regulates histone H3 trimethylation and gene expression by interaction with the polycomb protein EED/WAIT1

RETRACTED: PINK1 regulates histone H3 trimethylation and gene expression by interaction with the polycomb protein EED/WAIT1

The Putative Tumor Suppressor microRNA-101 Modulates the Cancer Epigenome by Repressing the Polycomb Group Protein EZH2

Interactive Roles of Ets-1, Sp1, and Acetylated Histones in the Retinoic Acid-dependent Activation of Guanylyl Cyclase/Atrial Natriuretic Peptide Receptor-A Gene Transcription

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