ADP-ribose polymers localized on Ctcf–Parp1–Dnmt1 complex prevent methylation of Ctcf target sites

Zampieri, Michele; Guastafierro, Tiziana; Calabrese, R.; Ciccarone, Fabio; Bacalini, Maria Giulia; Reale, Anna; Perilli, Mariagrazia; Passananti, Claudio; Caiafa, Paola

doi:10.1042/bj20111417

Cited by 109 publications

(108 citation statements)

References 51 publications

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“…This could be facilitated by inhibition of DNA methyl-transferases (both de novo enzymes DNMT3A and B and maintenance enzyme DNMT1). Indeed, PARP1 has been suggested to be implicated in regulation of DNMT1 (Zampieri et al, 2012, Zampieri et al, 2009) together with UHRF1 (Bostick et al, 2007).…”

Section: Colonizationmentioning

confidence: 99%

Epigenetic features of testicular germ cell tumours in relation to epigenetic characteristics of foetal germ cells

Kristensen¹,

Skakkebæk²,

Meyts³

et al. 2013

Int. J. Dev. Biol.

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Foetal development of germ cells is a unique biological process orchestrated by cellular specification, migration and niche development in concert with extensive epigenetic and transcriptional programs. Many of these processes take place early in foetal life and are hence very difficult to study in humans. However, the common precursor of testicular cancers -the carcinoma in situ (CIS) cell -is thought to be an arrested foetal germ cell. Therefore studies of CIS cells may leverage information on human foetal germ cell development and, in particular, when neoplastic transformation is initiated. In this review, we will focus on current knowledge of the epigenetics of CIS cells and relate it to the epigenetic changes occurring in early developing germ cells of mice during specification, migration and colonization. We will focus on DNA methylation and some of the best studied histone modifications like H3K9me2, H3K27me3 and H3K9ac. We also show that CIS cells contain high levels of H3K27ac, which is known to mark active enhancers. Proper epigenetic reprogramming seems to be a pre-requisite of normal foetal germ cell development and we propose that alterations in these programs may be a pathogenic event in the initiation of testicular germ cell cancer. Even though only sparse information is available on epigenetic cues in human foetal germ cells, these indicate that the developmental patterns differ from the findings in mice and emphasize the need for further studies of foetal germ cell development in humans.

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Section: Colonizationmentioning

confidence: 99%

Epigenetic features of testicular germ cell tumours in relation to epigenetic characteristics of foetal germ cells

Kristensen¹,

Skakkebæk²,

Meyts³

et al. 2013

Int. J. Dev. Biol.

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“…Moreover, CTCF can influence DNA methylation by forming a complex with two enzymes related to DNA methylation: poly(ADP-ribose) polymerase 1 (PARP1) and the ubiquitously expressed DNA (cytosine-5)-methyltransferase 1 (DNMT1). CTCF activates PARP1, which then can add ADP -ribose groups to DNMT1 to inactivate this enzyme, with maintenance of methyl-free CpGs as the result [30][31][32].…”

Section: Ctcf Binds Across the Genome To Chromatin Boundaries Enhancmentioning

confidence: 99%

CTCF: the protein, the binding partners, the binding sites and their chromatin loops

Holwerda

Laat

2013

Phil. Trans. R. Soc. B

190

161

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CTCF has it all. The transcription factor binds to tens of thousands of genomic sites, some tissue-specific, others ultra-conserved. It can act as a transcriptional activator, repressor and insulator, and it can pause transcription. CTCF binds at chromatin domain boundaries, at enhancers and gene promoters, and inside gene bodies. It can attract many other transcription factors to chromatin, including tissue-specific transcriptional activators, repressors, cohesin and RNA polymerase II, and it forms chromatin loops. Yet, or perhaps therefore, CTCF's exact function at a given genomic site is unpredictable. It appears to be determined by the associated transcription factors, by the location of the binding site relative to the transcriptional start site of a gene, and by the site's engagement in chromatin loops with other CTCF-binding sites, enhancers or gene promoters. Here, we will discuss genome-wide features of CTCF binding events, as well as locus-specific functions of this remarkable transcription factor.

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“…The chromatin insulator CTCF (CCCTC-binding factor) is another important regulator of gene transcription and chromatin structure. CTCF is able to activate PARP1 which then forms a complex with DNMT1 and inhibits its methylase activity at CTCF-bound CpGs [200]. Recent evidence suggests that not only methylation is regulated by PARylation, but also the demethylation process is under PARylation control.…”

Section: Chromatin Regulation Epigenetics and Transcriptionmentioning

confidence: 99%

Multitasking Roles for Poly(ADP-ribosyl)ation in Aging and Longevity

Mangerich

Bürkle

2015

Cancer Drug Discovery and Development

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Aging is a multifactorial process that depends on diverse molecular and cellular mechanisms, such as genome instability, epigenetic and transcriptional changes, loss of proteostasis, cell death and senescence, metabolic dysfunction, and inflammation. Enzymes of the family of poly(ADP-ribose) polymerases (PARPs) catalyze the synthesis of the biopolymer poly(ADP-ribose) (PAR), a drastic posttranslational modification that plays significant roles in all of these processes. On the one hand, poly(ADP-ribosyl)ation (PARylation) contributes to genome and proteome homeostasis, as it participates in chromatin remodeling, genome maintenance, cell cycle control, and the regulation of the ubiquitin-proteasome system. On the other hand, PARPs and PARylation interfere with cellular and organismic energy metabolism, and act as mediators of inflammation, senescence and cell death. Therefore, PARylation is discussed both as a longevity assurance factor on the one hand and an aging-promoting factor on the other hand. Here we highlight the mechanisms underlying the various roles of PARylation in longevity and aging with a focus on molecular and cellular mechanisms.

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ADP-ribose polymers localized on Ctcf–Parp1–Dnmt1 complex prevent methylation of Ctcf target sites

Cited by 109 publications

References 51 publications

Epigenetic features of testicular germ cell tumours in relation to epigenetic characteristics of foetal germ cells

Epigenetic features of testicular germ cell tumours in relation to epigenetic characteristics of foetal germ cells

CTCF: the protein, the binding partners, the binding sites and their chromatin loops

Multitasking Roles for Poly(ADP-ribosyl)ation in Aging and Longevity

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