H3K4me3 demethylation by the histone demethylase KDM5C/JARID1C promotes DNA replication origin firing

Rondinelli, Beatrice; Schwerer, Hélène; Antonini, Elena; Gaviraghi, Marco; Lupi, Alessio; Frenquelli, Michela; Cittaro, Davide; Segalla, Simona; Lemaı̂tre, Jean-Marc; Tonon, Giovanni

doi:10.1093/nar/gkv090

Cited by 54 publications

(53 citation statements)

References 75 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Along similar lines, in renal cancer cell lines, JARID1C also comprehensively regulates H3K4me3 levels (47). Additionally, we have recently identified a nontranscriptional role for JARID1C in DNA replication (48).…”

Section: Introductionmentioning

confidence: 69%

Histone demethylase JARID1C inactivation triggers genomic instability in sporadic renal cancer

Rondinelli

Rosano

Antonini

et al. 2015

Journal of Clinical Investigation

Self Cite

View full text Add to dashboard Cite

Section: Introductionmentioning

confidence: 69%

Histone demethylase JARID1C inactivation triggers genomic instability in sporadic renal cancer

Rondinelli

Rosano

Antonini

et al. 2015

Journal of Clinical Investigation

Self Cite

View full text Add to dashboard Cite

“…Then, it turns to nucleus to regulate transcription factors such as c-myc, NF-κB, and promote the transcription of genes responsible for the process of cellular proliferation and apoptosis. Over proliferation of gastric mucosal cell was also accompanied by over-expression of PCNA22 that firmly tethers polymerases to DNA and increase their processivity for tens to thousands of nucleotides. The expression level of PCNA increases with degree of epithelial cell hyperplasia which reflects the state of cellular proliferation.…”

Section: Resultsmentioning

confidence: 99%

NMR-based metabolomics Reveals Alterations of Electro-acupuncture Stimulations on Chronic Atrophic Gastritis Rats

Zheng

Cheng

et al. 2017

Sci Rep

View full text Add to dashboard Cite

Chronic atrophic gastritis (CAG) is a common gastrointestinal disease which has been considered as precancerous lesions of gastric carcinoma. Previously, electro-acupuncture stimulation has been shown to be effective in ameliorating symptoms of CAG. However the underlying mechanism of this beneficial treatment is yet to be established. In the present study, an integrated histopathological examination along with molecular biological assay, as well as 1H NMR analysis of multiple biological samples (urine, serum, stomach, cortex and medulla) were employed to systematically assess the pathology of CAG and therapeutic effect of electro-acupuncture stimulation at Sibai (ST 2), Liangmen (ST 21), and Zusanli (ST 36) acupoints located in the stomach meridian using a rat model of CAG. The current results showed that CAG caused comprehensive metabolic alterations including the TCA cycle, glycolysis, membrane metabolism and catabolism, gut microbiota-related metabolism. On the other hand, electro-acupuncture treatment was found able to normalize a number of CAG-induced metabolomics changes by alleviating membrane catabolism, restoring function of neurotransmitter in brain and partially reverse the CAG-induced perturbation in gut microbiota metabolism. These findings provided new insights into the biochemistry of CAG and mechanism of the therapeutic effect of electro-acupuncture stimulations.

show abstract

“…Given their near-universal presence at ORC2 sites, acetylated H3 and/or dimethylated H3K4 are excellent candidates to be recognized by ORC. H3K4 dimethylation promotes replication origin function in yeast (49), and H34K4me3 demethylation promotes replication origin firing (50), although the mechanism is unknown. However, the ORC subunits do not contain previously identified domains for interacting with these histone modifications.…”

Section: Discussionmentioning

confidence: 99%

Selectivity of ORC binding sites and the relation to replication timing, fragile sites, and deletions in cancers

Miotto

Struhl

2016

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

176

216

View full text Add to dashboard Cite

The origin recognition complex (ORC) binds sites from which DNA replication is initiated. We address ORC binding selectivity in vivo by mapping ∼52,000 ORC2 binding sites throughout the human genome. The ORC binding profile is broader than those of sequence-specific transcription factors, suggesting that ORC is not bound or recruited to specific DNA sequences. Instead, ORC binds nonspecifically to open (DNase I-hypersensitive) regions containing active chromatin marks such as H3 acetylation and H3K4 methylation. ORC sites in early and late replicating regions have similar properties, but there are far more ORC sites in early replicating regions. This suggests that replication timing is due primarily to ORC density and stochastic firing of origins. Computational simulation of stochastic firing from identified ORC sites is in accord with replication timing data. Large genomic regions with a paucity of ORC sites are strongly associated with common fragile sites and recurrent deletions in cancers. We suggest that replication origins, replication timing, and replication-dependent chromosome breaks are determined primarily by the genomic distribution of activator proteins at enhancers and promoters. These activators recruit nucleosome-modifying complexes to create the appropriate chromatin structure that allows ORC binding and subsequent origin firing.DNA replication | replication origins | chromatin | replication timing | ORC R eplication origins are established by the assembly of the prereplication complex at discrete sites of the genome. The first step of this process involves binding of the highly conserved six-subunit origin recognition complex (ORC), which serves as a loading platform for the subsequent assembly of helicases, DNA polymerases, and cofactors required for DNA synthesis (1, 2). In the yeast Saccharomyces cerevisiae, ORC binds DNA in an ATP-dependent manner and recognizes a specific DNA sequence (3). In Drosophila, ORC localizes to regions of open chromatin with contributions from activating histone modifications, DNA sequence, DNA binding proteins, and nucleosome remodelers (4-6). In mammals, the mechanism(s) through which ORC is localized and establishes a functional origin remains unclear.A great deal of effort and a variety of experimental approaches have been devoted to describing the nature and position of replication origins in mammalian genomes. DNA combing technology, replication timing analysis, short nascent strand (SNS) enrichment, and bubble trapping approaches suggest that DNA replication initiation sites are enriched in CpG-rich regions, open chromatin domains, and transcriptional regulatory elements (7-17). However, these methods lack the necessary resolution to investigate important relationships of ORC binding with other features of the genome. In addition, the divergence in protocols and bioinformatic pipelines between laboratories has led to some controversial and nonreproducible observations. Finally, these studies assume that the identified replication initiation sites are compa...

show abstract

H3K4me3 demethylation by the histone demethylase KDM5C/JARID1C promotes DNA replication origin firing

Cited by 54 publications

References 75 publications

Histone demethylase JARID1C inactivation triggers genomic instability in sporadic renal cancer

Histone demethylase JARID1C inactivation triggers genomic instability in sporadic renal cancer

NMR-based metabolomics Reveals Alterations of Electro-acupuncture Stimulations on Chronic Atrophic Gastritis Rats

Selectivity of ORC binding sites and the relation to replication timing, fragile sites, and deletions in cancers

Contact Info

Product

Resources

About