Selectivity of ORC binding sites and the relation to replication timing, fragile sites, and deletions in cancers
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...
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| Autor*in: |
Miotto, Benoit [verfasserIn] |
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| Format: |
Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2016 |
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| Rechteinformationen: |
Nutzungsrecht: © COPYRIGHT 2016 National Academy of Sciences |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Proceedings of the National Academy of Sciences of the United States of America - Washington, DC : NAS, 1877, 113(2016), 33, Seite E4810-E4819 |
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| Übergeordnetes Werk: |
volume:113 ; year:2016 ; number:33 ; pages:E4810-E4819 |
| Links: |
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| DOI / URN: |
10.1073/pnas.1609060113 |
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| 520 | |a 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. | ||
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| 650 | 4 | |a DNA replication | |
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10.1073/pnas.1609060113 doi PQ20161201 (DE-627)OLC1986415341 (DE-599)GBVOLC1986415341 (PRQ)c1740-3c698e43b33fa0dde498947b2f082aee0843e3cf3aaa7b4bc9308b3bbc12cbfa0 (KEY)0583363920160000113003304810selectivityoforcbindingsitesandtherelationtoreplic DE-627 ger DE-627 rakwb eng 500 DNB 570 AVZ LING fid BIODIV fid Miotto, Benoit verfasserin aut Selectivity of ORC binding sites and the relation to replication timing, fragile sites, and deletions in cancers 2016 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier 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. Nutzungsrecht: © COPYRIGHT 2016 National Academy of Sciences DNA sequencing DNA replication Binding sites (Biochemistry) Health aspects Nucleotide sequencing Methods Genomes Chromosomes Chromatin Binding sites Deoxyribonucleic acid--DNA Proteins Simulation Ji, Zhe oth Struhl, Kevin oth Enthalten in Proceedings of the National Academy of Sciences of the United States of America Washington, DC : NAS, 1877 113(2016), 33, Seite E4810-E4819 (DE-627)129505269 (DE-600)209104-5 (DE-576)014909189 0027-8424 nnns volume:113 year:2016 number:33 pages:E4810-E4819 http://dx.doi.org/10.1073/pnas.1609060113 Volltext http://www.ncbi.nlm.nih.gov/pubmed/27436900 http://search.proquest.com/docview/1813624739 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-MAT SSG-OPC-FOR GBV_ILN_40 GBV_ILN_59 AR 113 2016 33 E4810-E4819 |
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10.1073/pnas.1609060113 doi PQ20161201 (DE-627)OLC1986415341 (DE-599)GBVOLC1986415341 (PRQ)c1740-3c698e43b33fa0dde498947b2f082aee0843e3cf3aaa7b4bc9308b3bbc12cbfa0 (KEY)0583363920160000113003304810selectivityoforcbindingsitesandtherelationtoreplic DE-627 ger DE-627 rakwb eng 500 DNB 570 AVZ LING fid BIODIV fid Miotto, Benoit verfasserin aut Selectivity of ORC binding sites and the relation to replication timing, fragile sites, and deletions in cancers 2016 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier 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. Nutzungsrecht: © COPYRIGHT 2016 National Academy of Sciences DNA sequencing DNA replication Binding sites (Biochemistry) Health aspects Nucleotide sequencing Methods Genomes Chromosomes Chromatin Binding sites Deoxyribonucleic acid--DNA Proteins Simulation Ji, Zhe oth Struhl, Kevin oth Enthalten in Proceedings of the National Academy of Sciences of the United States of America Washington, DC : NAS, 1877 113(2016), 33, Seite E4810-E4819 (DE-627)129505269 (DE-600)209104-5 (DE-576)014909189 0027-8424 nnns volume:113 year:2016 number:33 pages:E4810-E4819 http://dx.doi.org/10.1073/pnas.1609060113 Volltext http://www.ncbi.nlm.nih.gov/pubmed/27436900 http://search.proquest.com/docview/1813624739 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-MAT SSG-OPC-FOR GBV_ILN_40 GBV_ILN_59 AR 113 2016 33 E4810-E4819 |
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10.1073/pnas.1609060113 doi PQ20161201 (DE-627)OLC1986415341 (DE-599)GBVOLC1986415341 (PRQ)c1740-3c698e43b33fa0dde498947b2f082aee0843e3cf3aaa7b4bc9308b3bbc12cbfa0 (KEY)0583363920160000113003304810selectivityoforcbindingsitesandtherelationtoreplic DE-627 ger DE-627 rakwb eng 500 DNB 570 AVZ LING fid BIODIV fid Miotto, Benoit verfasserin aut Selectivity of ORC binding sites and the relation to replication timing, fragile sites, and deletions in cancers 2016 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier 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. Nutzungsrecht: © COPYRIGHT 2016 National Academy of Sciences DNA sequencing DNA replication Binding sites (Biochemistry) Health aspects Nucleotide sequencing Methods Genomes Chromosomes Chromatin Binding sites Deoxyribonucleic acid--DNA Proteins Simulation Ji, Zhe oth Struhl, Kevin oth Enthalten in Proceedings of the National Academy of Sciences of the United States of America Washington, DC : NAS, 1877 113(2016), 33, Seite E4810-E4819 (DE-627)129505269 (DE-600)209104-5 (DE-576)014909189 0027-8424 nnns volume:113 year:2016 number:33 pages:E4810-E4819 http://dx.doi.org/10.1073/pnas.1609060113 Volltext http://www.ncbi.nlm.nih.gov/pubmed/27436900 http://search.proquest.com/docview/1813624739 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-MAT SSG-OPC-FOR GBV_ILN_40 GBV_ILN_59 AR 113 2016 33 E4810-E4819 |
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10.1073/pnas.1609060113 doi PQ20161201 (DE-627)OLC1986415341 (DE-599)GBVOLC1986415341 (PRQ)c1740-3c698e43b33fa0dde498947b2f082aee0843e3cf3aaa7b4bc9308b3bbc12cbfa0 (KEY)0583363920160000113003304810selectivityoforcbindingsitesandtherelationtoreplic DE-627 ger DE-627 rakwb eng 500 DNB 570 AVZ LING fid BIODIV fid Miotto, Benoit verfasserin aut Selectivity of ORC binding sites and the relation to replication timing, fragile sites, and deletions in cancers 2016 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier 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. Nutzungsrecht: © COPYRIGHT 2016 National Academy of Sciences DNA sequencing DNA replication Binding sites (Biochemistry) Health aspects Nucleotide sequencing Methods Genomes Chromosomes Chromatin Binding sites Deoxyribonucleic acid--DNA Proteins Simulation Ji, Zhe oth Struhl, Kevin oth Enthalten in Proceedings of the National Academy of Sciences of the United States of America Washington, DC : NAS, 1877 113(2016), 33, Seite E4810-E4819 (DE-627)129505269 (DE-600)209104-5 (DE-576)014909189 0027-8424 nnns volume:113 year:2016 number:33 pages:E4810-E4819 http://dx.doi.org/10.1073/pnas.1609060113 Volltext http://www.ncbi.nlm.nih.gov/pubmed/27436900 http://search.proquest.com/docview/1813624739 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-MAT SSG-OPC-FOR GBV_ILN_40 GBV_ILN_59 AR 113 2016 33 E4810-E4819 |
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selectivity of orc binding sites and the relation to replication timing, fragile sites, and deletions in cancers |
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Selectivity of ORC binding sites and the relation to replication timing, fragile sites, and deletions in cancers |
| abstract |
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. |
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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. |
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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. |
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Selectivity of ORC binding sites and the relation to replication timing, fragile sites, and deletions in cancers |
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