Genomic instability and endoreduplication triggered by RAD17 deletion
Cell cycle checkpoints are critical for genomic stability. Rad17, a component of the checkpoint clamp loader complex (Rad17/Rfc2-5), is required for the response to DNA damage and replication stress. To explore the role of Rad17 in the maintenance of genomic integrity, we established somatic conditi...
Gespeichert in:
| Veröffentlicht in: | Genes & development 2003-04, Vol.17 (8), p.965-970 |
|---|---|
| Hauptverfasser: | , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 970 |
|---|---|
| container_issue | 8 |
| container_start_page | 965 |
| container_title | Genes & development |
| container_volume | 17 |
| creator | Wang, Xin Zou, Lee Zheng, Huyong Wei, Qingyi Elledge, Stephen J Li, Lei |
| description | Cell cycle checkpoints are critical for genomic stability. Rad17, a component of the checkpoint clamp loader complex (Rad17/Rfc2-5), is required for the response to DNA damage and replication stress. To explore the role of Rad17 in the maintenance of genomic integrity, we established somatic conditional alleles of RAD17 in human cells. We find that RAD17 is not only important for the Atr-mediated checkpoint but is also essential for cell viability. Cells lacking RAD17 exhibited acute chromosomal aberrations and underwent endoreduplication at a high rate. Therefore, RAD17 links the checkpoint to ploidy control and is essential for the maintenance of chromosomal stability. |
| doi_str_mv | 10.1101/gad.1065103 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_196036</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>18765916</sourcerecordid><originalsourceid>FETCH-LOGICAL-c370t-b3dc2c0f28f32a77e14fffc1ee94cbf65c3ba93f40c93b9d9b9a81b912db0c923</originalsourceid><addsrcrecordid>eNqFkUtLw0AUhQdRbH2s3EtWbiR17kwy01m4KLVWoSCIrod5xpE0qZlE6L83pcHHytWFc79zOHAQugA8AcBwUyg7AcxywPQAjSHPRJpnnB-iMZ4KnArKxAidxPiOMWaYsWM0AsI4YQKP0WLpqnodTBKq2CodytBuE1XZxFW2bpztNmUwqg11lbRNKArXa4neJs-zO-CJdaXb_c7QkVdldOfDPUWv94uX-UO6elo-zmer1FCO21RTa4jBnkw9JYpzB5n33oBzIjPas9xQrQT1GTaCamGFFmoKWgCxupcIPUW3-9xNp9fOGle1jSrlpglr1WxlrYL8-6nCmyzqTwmCYcp6_9Xgb-qPzsVWrkM0rixV5eouSk4J4UD5vyBMOcsF7BKv96Bp6hgb57_LAJa7eWQ_jxzm6enL3_1_2GEP-gVh4oz5</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>18765916</pqid></control><display><type>article</type><title>Genomic instability and endoreduplication triggered by RAD17 deletion</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><creator>Wang, Xin ; Zou, Lee ; Zheng, Huyong ; Wei, Qingyi ; Elledge, Stephen J ; Li, Lei</creator><creatorcontrib>Wang, Xin ; Zou, Lee ; Zheng, Huyong ; Wei, Qingyi ; Elledge, Stephen J ; Li, Lei</creatorcontrib><description>Cell cycle checkpoints are critical for genomic stability. Rad17, a component of the checkpoint clamp loader complex (Rad17/Rfc2-5), is required for the response to DNA damage and replication stress. To explore the role of Rad17 in the maintenance of genomic integrity, we established somatic conditional alleles of RAD17 in human cells. We find that RAD17 is not only important for the Atr-mediated checkpoint but is also essential for cell viability. Cells lacking RAD17 exhibited acute chromosomal aberrations and underwent endoreduplication at a high rate. Therefore, RAD17 links the checkpoint to ploidy control and is essential for the maintenance of chromosomal stability.</description><identifier>ISSN: 0890-9369</identifier><identifier>EISSN: 1549-5477</identifier><identifier>DOI: 10.1101/gad.1065103</identifier><identifier>PMID: 12672690</identifier><language>eng</language><publisher>United States: Cold Spring Harbor Laboratory Press</publisher><subject>Blotting, Southern ; Blotting, Western ; Cell Cycle - physiology ; Cell Cycle Proteins - physiology ; Cell Survival ; Cells, Cultured ; Chromosome Aberrations ; Colon - pathology ; DNA Damage ; Epithelial Cells - pathology ; Exodeoxyribonucleases ; Gene Deletion ; Gene Duplication ; Humans ; Integrases - metabolism ; Karyotyping ; Phosphoproteins - metabolism ; Phosphorylation ; Research Communication ; Transfection ; Viral Proteins - metabolism</subject><ispartof>Genes & development, 2003-04, Vol.17 (8), p.965-970</ispartof><rights>Copyright © 2003, Cold Spring Harbor Laboratory Press 2003</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c370t-b3dc2c0f28f32a77e14fffc1ee94cbf65c3ba93f40c93b9d9b9a81b912db0c923</citedby><cites>FETCH-LOGICAL-c370t-b3dc2c0f28f32a77e14fffc1ee94cbf65c3ba93f40c93b9d9b9a81b912db0c923</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/PMC196036/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC196036/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12672690$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Xin</creatorcontrib><creatorcontrib>Zou, Lee</creatorcontrib><creatorcontrib>Zheng, Huyong</creatorcontrib><creatorcontrib>Wei, Qingyi</creatorcontrib><creatorcontrib>Elledge, Stephen J</creatorcontrib><creatorcontrib>Li, Lei</creatorcontrib><title>Genomic instability and endoreduplication triggered by RAD17 deletion</title><title>Genes & development</title><addtitle>Genes Dev</addtitle><description>Cell cycle checkpoints are critical for genomic stability. Rad17, a component of the checkpoint clamp loader complex (Rad17/Rfc2-5), is required for the response to DNA damage and replication stress. To explore the role of Rad17 in the maintenance of genomic integrity, we established somatic conditional alleles of RAD17 in human cells. We find that RAD17 is not only important for the Atr-mediated checkpoint but is also essential for cell viability. Cells lacking RAD17 exhibited acute chromosomal aberrations and underwent endoreduplication at a high rate. Therefore, RAD17 links the checkpoint to ploidy control and is essential for the maintenance of chromosomal stability.</description><subject>Blotting, Southern</subject><subject>Blotting, Western</subject><subject>Cell Cycle - physiology</subject><subject>Cell Cycle Proteins - physiology</subject><subject>Cell Survival</subject><subject>Cells, Cultured</subject><subject>Chromosome Aberrations</subject><subject>Colon - pathology</subject><subject>DNA Damage</subject><subject>Epithelial Cells - pathology</subject><subject>Exodeoxyribonucleases</subject><subject>Gene Deletion</subject><subject>Gene Duplication</subject><subject>Humans</subject><subject>Integrases - metabolism</subject><subject>Karyotyping</subject><subject>Phosphoproteins - metabolism</subject><subject>Phosphorylation</subject><subject>Research Communication</subject><subject>Transfection</subject><subject>Viral Proteins - metabolism</subject><issn>0890-9369</issn><issn>1549-5477</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUtLw0AUhQdRbH2s3EtWbiR17kwy01m4KLVWoSCIrod5xpE0qZlE6L83pcHHytWFc79zOHAQugA8AcBwUyg7AcxywPQAjSHPRJpnnB-iMZ4KnArKxAidxPiOMWaYsWM0AsI4YQKP0WLpqnodTBKq2CodytBuE1XZxFW2bpztNmUwqg11lbRNKArXa4neJs-zO-CJdaXb_c7QkVdldOfDPUWv94uX-UO6elo-zmer1FCO21RTa4jBnkw9JYpzB5n33oBzIjPas9xQrQT1GTaCamGFFmoKWgCxupcIPUW3-9xNp9fOGle1jSrlpglr1WxlrYL8-6nCmyzqTwmCYcp6_9Xgb-qPzsVWrkM0rixV5eouSk4J4UD5vyBMOcsF7BKv96Bp6hgb57_LAJa7eWQ_jxzm6enL3_1_2GEP-gVh4oz5</recordid><startdate>20030415</startdate><enddate>20030415</enddate><creator>Wang, Xin</creator><creator>Zou, Lee</creator><creator>Zheng, Huyong</creator><creator>Wei, Qingyi</creator><creator>Elledge, Stephen J</creator><creator>Li, Lei</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>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20030415</creationdate><title>Genomic instability and endoreduplication triggered by RAD17 deletion</title><author>Wang, Xin ; Zou, Lee ; Zheng, Huyong ; Wei, Qingyi ; Elledge, Stephen J ; Li, Lei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c370t-b3dc2c0f28f32a77e14fffc1ee94cbf65c3ba93f40c93b9d9b9a81b912db0c923</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Blotting, Southern</topic><topic>Blotting, Western</topic><topic>Cell Cycle - physiology</topic><topic>Cell Cycle Proteins - physiology</topic><topic>Cell Survival</topic><topic>Cells, Cultured</topic><topic>Chromosome Aberrations</topic><topic>Colon - pathology</topic><topic>DNA Damage</topic><topic>Epithelial Cells - pathology</topic><topic>Exodeoxyribonucleases</topic><topic>Gene Deletion</topic><topic>Gene Duplication</topic><topic>Humans</topic><topic>Integrases - metabolism</topic><topic>Karyotyping</topic><topic>Phosphoproteins - metabolism</topic><topic>Phosphorylation</topic><topic>Research Communication</topic><topic>Transfection</topic><topic>Viral Proteins - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Xin</creatorcontrib><creatorcontrib>Zou, Lee</creatorcontrib><creatorcontrib>Zheng, Huyong</creatorcontrib><creatorcontrib>Wei, Qingyi</creatorcontrib><creatorcontrib>Elledge, Stephen J</creatorcontrib><creatorcontrib>Li, Lei</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</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>Wang, Xin</au><au>Zou, Lee</au><au>Zheng, Huyong</au><au>Wei, Qingyi</au><au>Elledge, Stephen J</au><au>Li, Lei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Genomic instability and endoreduplication triggered by RAD17 deletion</atitle><jtitle>Genes & development</jtitle><addtitle>Genes Dev</addtitle><date>2003-04-15</date><risdate>2003</risdate><volume>17</volume><issue>8</issue><spage>965</spage><epage>970</epage><pages>965-970</pages><issn>0890-9369</issn><eissn>1549-5477</eissn><abstract>Cell cycle checkpoints are critical for genomic stability. Rad17, a component of the checkpoint clamp loader complex (Rad17/Rfc2-5), is required for the response to DNA damage and replication stress. To explore the role of Rad17 in the maintenance of genomic integrity, we established somatic conditional alleles of RAD17 in human cells. We find that RAD17 is not only important for the Atr-mediated checkpoint but is also essential for cell viability. Cells lacking RAD17 exhibited acute chromosomal aberrations and underwent endoreduplication at a high rate. Therefore, RAD17 links the checkpoint to ploidy control and is essential for the maintenance of chromosomal stability.</abstract><cop>United States</cop><pub>Cold Spring Harbor Laboratory Press</pub><pmid>12672690</pmid><doi>10.1101/gad.1065103</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0890-9369 |
| ispartof | Genes & development, 2003-04, Vol.17 (8), p.965-970 |
| issn | 0890-9369 1549-5477 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_196036 |
| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Blotting, Southern Blotting, Western Cell Cycle - physiology Cell Cycle Proteins - physiology Cell Survival Cells, Cultured Chromosome Aberrations Colon - pathology DNA Damage Epithelial Cells - pathology Exodeoxyribonucleases Gene Deletion Gene Duplication Humans Integrases - metabolism Karyotyping Phosphoproteins - metabolism Phosphorylation Research Communication Transfection Viral Proteins - metabolism |
| title | Genomic instability and endoreduplication triggered by RAD17 deletion |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-13T22%3A04%3A56IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Genomic%20instability%20and%20endoreduplication%20triggered%20by%20RAD17%20deletion&rft.jtitle=Genes%20&%20development&rft.au=Wang,%20Xin&rft.date=2003-04-15&rft.volume=17&rft.issue=8&rft.spage=965&rft.epage=970&rft.pages=965-970&rft.issn=0890-9369&rft.eissn=1549-5477&rft_id=info:doi/10.1101/gad.1065103&rft_dat=%3Cproquest_pubme%3E18765916%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=18765916&rft_id=info:pmid/12672690&rfr_iscdi=true |