The role of PR-Set7 in replication licensing depends on Suv4-20h
PR-Set7 is the sole monomethyltransferase responsible for H4K20 monomethylation (H4K20me1) that is the substrate for further methylation by Suv4-20h1/h2. PR-Set7 is required for proper cell cycle progression and is subject to degradation by the CRL4(Cdt2) ubiquitin ligase complex as a function of th...
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| Veröffentlicht in: | Genes & development 2012-12, Vol.26 (23), p.2580-2589 |
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| creator | Beck, David B Burton, Adam Oda, Hisanobu Ziegler-Birling, Céline Torres-Padilla, Maria-Elena Reinberg, Danny |
| description | PR-Set7 is the sole monomethyltransferase responsible for H4K20 monomethylation (H4K20me1) that is the substrate for further methylation by Suv4-20h1/h2. PR-Set7 is required for proper cell cycle progression and is subject to degradation by the CRL4(Cdt2) ubiquitin ligase complex as a function of the cell cycle and DNA damage. This report demonstrates that PR-Set7 is an important downstream effector of CRL4(Cdt2) function during origin of DNA replication licensing, dependent on Suv4-20h1/2 activity. Aberrant rereplication correlates with decreased levels of H4K20me1 and increased levels of H4K20 trimethylation (H4K20me3). Expression of a degradation-resistant PR-Set7 mutant in the mouse embryo that is normally devoid of Suv4-20 does not compromise development or cell cycle progression unless Suv4-20h is coexpressed. PR-Set7 targeting to an artificial locus results in recruitment of the origin recognition complex (ORC) in a manner dependent on Suv4-20h and H4K20me3. Consistent with this, H4K20 methylation status plays a direct role in recruiting ORC through the binding properties of ORC1 and ORCA/LRWD1. Thus, coordinating the status of H4K20 methylation is pivotal for the proper selection of DNA replication origins in higher eukaryotes. |
| doi_str_mv | 10.1101/gad.195636.112 |
| format | Article |
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PR-Set7 is required for proper cell cycle progression and is subject to degradation by the CRL4(Cdt2) ubiquitin ligase complex as a function of the cell cycle and DNA damage. This report demonstrates that PR-Set7 is an important downstream effector of CRL4(Cdt2) function during origin of DNA replication licensing, dependent on Suv4-20h1/2 activity. Aberrant rereplication correlates with decreased levels of H4K20me1 and increased levels of H4K20 trimethylation (H4K20me3). Expression of a degradation-resistant PR-Set7 mutant in the mouse embryo that is normally devoid of Suv4-20 does not compromise development or cell cycle progression unless Suv4-20h is coexpressed. PR-Set7 targeting to an artificial locus results in recruitment of the origin recognition complex (ORC) in a manner dependent on Suv4-20h and H4K20me3. Consistent with this, H4K20 methylation status plays a direct role in recruiting ORC through the binding properties of ORC1 and ORCA/LRWD1. Thus, coordinating the status of H4K20 methylation is pivotal for the proper selection of DNA replication origins in higher eukaryotes.</description><identifier>ISSN: 0890-9369</identifier><identifier>EISSN: 1549-5477</identifier><identifier>DOI: 10.1101/gad.195636.112</identifier><identifier>PMID: 23152447</identifier><language>eng</language><publisher>United States: Cold Spring Harbor Laboratory Press</publisher><subject>Animals ; Cell Cycle - genetics ; Cell Cycle - physiology ; Cell Differentiation ; Cell Line, Tumor ; Cell Proliferation ; DNA Damage ; DNA Replication - genetics ; DNA Replication - physiology ; Embryo, Mammalian ; Fibroblasts - cytology ; Genetics ; HeLa Cells ; Histone-Lysine N-Methyltransferase - genetics ; Histone-Lysine N-Methyltransferase - metabolism ; Humans ; Life Sciences ; Mice ; Origin Recognition Complex - metabolism ; Protein Binding ; Research Paper ; Ubiquitin-Protein Ligases - metabolism</subject><ispartof>Genes & development, 2012-12, Vol.26 (23), p.2580-2589</ispartof><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><rights>Copyright © 2012 by Cold Spring Harbor Laboratory Press 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c490t-76fd479420056ade966368191a7ade983bef497bf68674da1a0fc6c4c441b5343</citedby><cites>FETCH-LOGICAL-c490t-76fd479420056ade966368191a7ade983bef497bf68674da1a0fc6c4c441b5343</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3521623/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3521623/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27922,27923,53789,53791</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23152447$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-04748011$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Beck, David B</creatorcontrib><creatorcontrib>Burton, Adam</creatorcontrib><creatorcontrib>Oda, Hisanobu</creatorcontrib><creatorcontrib>Ziegler-Birling, Céline</creatorcontrib><creatorcontrib>Torres-Padilla, Maria-Elena</creatorcontrib><creatorcontrib>Reinberg, Danny</creatorcontrib><title>The role of PR-Set7 in replication licensing depends on Suv4-20h</title><title>Genes & development</title><addtitle>Genes Dev</addtitle><description>PR-Set7 is the sole monomethyltransferase responsible for H4K20 monomethylation (H4K20me1) that is the substrate for further methylation by Suv4-20h1/h2. PR-Set7 is required for proper cell cycle progression and is subject to degradation by the CRL4(Cdt2) ubiquitin ligase complex as a function of the cell cycle and DNA damage. This report demonstrates that PR-Set7 is an important downstream effector of CRL4(Cdt2) function during origin of DNA replication licensing, dependent on Suv4-20h1/2 activity. Aberrant rereplication correlates with decreased levels of H4K20me1 and increased levels of H4K20 trimethylation (H4K20me3). Expression of a degradation-resistant PR-Set7 mutant in the mouse embryo that is normally devoid of Suv4-20 does not compromise development or cell cycle progression unless Suv4-20h is coexpressed. PR-Set7 targeting to an artificial locus results in recruitment of the origin recognition complex (ORC) in a manner dependent on Suv4-20h and H4K20me3. Consistent with this, H4K20 methylation status plays a direct role in recruiting ORC through the binding properties of ORC1 and ORCA/LRWD1. Thus, coordinating the status of H4K20 methylation is pivotal for the proper selection of DNA replication origins in higher eukaryotes.</description><subject>Animals</subject><subject>Cell Cycle - genetics</subject><subject>Cell Cycle - physiology</subject><subject>Cell Differentiation</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>DNA Damage</subject><subject>DNA Replication - genetics</subject><subject>DNA Replication - physiology</subject><subject>Embryo, Mammalian</subject><subject>Fibroblasts - cytology</subject><subject>Genetics</subject><subject>HeLa Cells</subject><subject>Histone-Lysine N-Methyltransferase - genetics</subject><subject>Histone-Lysine N-Methyltransferase - metabolism</subject><subject>Humans</subject><subject>Life Sciences</subject><subject>Mice</subject><subject>Origin Recognition Complex - metabolism</subject><subject>Protein Binding</subject><subject>Research Paper</subject><subject>Ubiquitin-Protein Ligases - metabolism</subject><issn>0890-9369</issn><issn>1549-5477</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdUctOwzAQtBCIlsKVI8oRDileP-MLoqqAIlUC0XK2nMRpg9IkxEkl_h5XKRWwF--sZ8ZrDUKXgMcAGG5XJh2D4oIKj8kRGgJnKuRMymM0xJHCoaJCDdCZcx8YY4GFOEUDQoETxuQQ3S_XNmiqwgZVFry-hQvbyiAvg8bWRZ6YNq_KwDe2dHm5ClJb2zJ1gR8uui0LCV6fo5PMFM5e7M8Ren98WE5n4fzl6Xk6mYcJU7gNpchSJhUjGHNhUquEXzkCBUbuUERjmzEl40xEQrLUgMFZIhKWMAYxp4yO0F3vW3fxxqZ-o7Yxha6bfGOaL12ZXP-9KfO1XlVbTTkBQag3uOkN1v9ks8lc72aYSRZhgC147vX-sab67Kxr9SZ3iS0KU9qqcxqIL8q5lJ467qlJUznX2OzgDVjvItI-It1H5DHxgqvfHznQfzKh39mFilQ</recordid><startdate>20121201</startdate><enddate>20121201</enddate><creator>Beck, David B</creator><creator>Burton, Adam</creator><creator>Oda, Hisanobu</creator><creator>Ziegler-Birling, Céline</creator><creator>Torres-Padilla, Maria-Elena</creator><creator>Reinberg, Danny</creator><general>Cold Spring Harbor Laboratory Press</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>1XC</scope><scope>5PM</scope></search><sort><creationdate>20121201</creationdate><title>The role of PR-Set7 in replication licensing depends on Suv4-20h</title><author>Beck, David B ; Burton, Adam ; Oda, Hisanobu ; Ziegler-Birling, Céline ; Torres-Padilla, Maria-Elena ; Reinberg, Danny</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c490t-76fd479420056ade966368191a7ade983bef497bf68674da1a0fc6c4c441b5343</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Animals</topic><topic>Cell Cycle - genetics</topic><topic>Cell Cycle - physiology</topic><topic>Cell Differentiation</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>DNA Damage</topic><topic>DNA Replication - genetics</topic><topic>DNA Replication - physiology</topic><topic>Embryo, Mammalian</topic><topic>Fibroblasts - cytology</topic><topic>Genetics</topic><topic>HeLa Cells</topic><topic>Histone-Lysine N-Methyltransferase - genetics</topic><topic>Histone-Lysine N-Methyltransferase - metabolism</topic><topic>Humans</topic><topic>Life Sciences</topic><topic>Mice</topic><topic>Origin Recognition Complex - metabolism</topic><topic>Protein Binding</topic><topic>Research Paper</topic><topic>Ubiquitin-Protein Ligases - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Beck, David B</creatorcontrib><creatorcontrib>Burton, Adam</creatorcontrib><creatorcontrib>Oda, Hisanobu</creatorcontrib><creatorcontrib>Ziegler-Birling, Céline</creatorcontrib><creatorcontrib>Torres-Padilla, Maria-Elena</creatorcontrib><creatorcontrib>Reinberg, Danny</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Genes & development</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Beck, David B</au><au>Burton, Adam</au><au>Oda, Hisanobu</au><au>Ziegler-Birling, Céline</au><au>Torres-Padilla, Maria-Elena</au><au>Reinberg, Danny</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The role of PR-Set7 in replication licensing depends on Suv4-20h</atitle><jtitle>Genes & development</jtitle><addtitle>Genes Dev</addtitle><date>2012-12-01</date><risdate>2012</risdate><volume>26</volume><issue>23</issue><spage>2580</spage><epage>2589</epage><pages>2580-2589</pages><issn>0890-9369</issn><eissn>1549-5477</eissn><abstract>PR-Set7 is the sole monomethyltransferase responsible for H4K20 monomethylation (H4K20me1) that is the substrate for further methylation by Suv4-20h1/h2. PR-Set7 is required for proper cell cycle progression and is subject to degradation by the CRL4(Cdt2) ubiquitin ligase complex as a function of the cell cycle and DNA damage. This report demonstrates that PR-Set7 is an important downstream effector of CRL4(Cdt2) function during origin of DNA replication licensing, dependent on Suv4-20h1/2 activity. Aberrant rereplication correlates with decreased levels of H4K20me1 and increased levels of H4K20 trimethylation (H4K20me3). Expression of a degradation-resistant PR-Set7 mutant in the mouse embryo that is normally devoid of Suv4-20 does not compromise development or cell cycle progression unless Suv4-20h is coexpressed. PR-Set7 targeting to an artificial locus results in recruitment of the origin recognition complex (ORC) in a manner dependent on Suv4-20h and H4K20me3. Consistent with this, H4K20 methylation status plays a direct role in recruiting ORC through the binding properties of ORC1 and ORCA/LRWD1. Thus, coordinating the status of H4K20 methylation is pivotal for the proper selection of DNA replication origins in higher eukaryotes.</abstract><cop>United States</cop><pub>Cold Spring Harbor Laboratory Press</pub><pmid>23152447</pmid><doi>10.1101/gad.195636.112</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Cell Cycle - genetics Cell Cycle - physiology Cell Differentiation Cell Line, Tumor Cell Proliferation DNA Damage DNA Replication - genetics DNA Replication - physiology Embryo, Mammalian Fibroblasts - cytology Genetics HeLa Cells Histone-Lysine N-Methyltransferase - genetics Histone-Lysine N-Methyltransferase - metabolism Humans Life Sciences Mice Origin Recognition Complex - metabolism Protein Binding Research Paper Ubiquitin-Protein Ligases - metabolism |
| title | The role of PR-Set7 in replication licensing depends on Suv4-20h |
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