Recruitment of Fanconi Anemia and Breast Cancer Proteins to DNA Damage Sites Is Differentially Governed by Replication
Fanconi anemia (FA) is characterized by cellular hypersensitivity to DNA crosslinking agents, but how the Fanconi pathway protects cells from DNA crosslinks and whether FA proteins act directly on crosslinks remain unclear. We developed a chromatin-IP-based strategy termed eChIP and detected associa...
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| Veröffentlicht in: | Molecular cell 2009-09, Vol.35 (5), p.716-723 |
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| creator | Shen, Xi Do, Huong Li, Yongjiang Chung, Woo-Hyun Tomasz, Maria de Winter, Johan P. Xia, Bing Elledge, Stephen J. Wang, Weidong Li, Lei |
| description | Fanconi anemia (FA) is characterized by cellular hypersensitivity to DNA crosslinking agents, but how the Fanconi pathway protects cells from DNA crosslinks and whether FA proteins act directly on crosslinks remain unclear. We developed a chromatin-IP-based strategy termed eChIP and detected association of multiple FA proteins with DNA crosslinks in vivo. Interdependence analyses revealed that crosslink-specific enrichment of various FA proteins is controlled by distinct mechanisms. BRCA-related FA proteins (BRCA2, FANCJ/BACH1, and FANCN/PALB2), but not FA core and I/D2 complexes, require replication for their crosslink association. FANCD2, but not FANCJ and FANCN, requires the FA core complex for its recruitment. FA core complex requires nucleotide excision repair proteins XPA and XPC for its association. Consistent with the distinct recruitment mechanism, recombination-independent crosslink repair was inversely affected in cells deficient of FANC-core versus BRCA-related FA proteins. Thus, FA proteins participate in distinct DNA damage response mechanisms governed by DNA replication status. |
| doi_str_mv | 10.1016/j.molcel.2009.06.034 |
| format | Article |
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We developed a chromatin-IP-based strategy termed eChIP and detected association of multiple FA proteins with DNA crosslinks in vivo. Interdependence analyses revealed that crosslink-specific enrichment of various FA proteins is controlled by distinct mechanisms. BRCA-related FA proteins (BRCA2, FANCJ/BACH1, and FANCN/PALB2), but not FA core and I/D2 complexes, require replication for their crosslink association. FANCD2, but not FANCJ and FANCN, requires the FA core complex for its recruitment. FA core complex requires nucleotide excision repair proteins XPA and XPC for its association. Consistent with the distinct recruitment mechanism, recombination-independent crosslink repair was inversely affected in cells deficient of FANC-core versus BRCA-related FA proteins. Thus, FA proteins participate in distinct DNA damage response mechanisms governed by DNA replication status.</description><identifier>ISSN: 1097-2765</identifier><identifier>EISSN: 1097-4164</identifier><identifier>DOI: 10.1016/j.molcel.2009.06.034</identifier><identifier>PMID: 19748364</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Apoptosis Regulatory Proteins ; Basic-Leucine Zipper Transcription Factors - genetics ; Basic-Leucine Zipper Transcription Factors - metabolism ; BRCA2 Protein - genetics ; BRCA2 Protein - metabolism ; Breast Neoplasms - genetics ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Cell Line, Tumor ; Chromatin Immunoprecipitation - methods ; Cross-Linking Reagents - pharmacology ; DNA ; DNA Damage ; DNA Replication ; DNA-Binding Proteins - metabolism ; Fanconi Anemia Complementation Group D2 Protein - genetics ; Fanconi Anemia Complementation Group D2 Protein - metabolism ; Fanconi Anemia Complementation Group N Protein ; Fanconi Anemia Complementation Group Proteins - genetics ; Fanconi Anemia Complementation Group Proteins - metabolism ; Female ; Ficusin - pharmacology ; Gene Expression Regulation, Neoplastic ; Humans ; Mutation ; Nuclear Proteins - genetics ; Nuclear Proteins - metabolism ; Plasmids - metabolism ; Recombination, Genetic ; Time Factors ; Tumor Suppressor Proteins - genetics ; Tumor Suppressor Proteins - metabolism ; Xeroderma Pigmentosum Group A Protein - metabolism</subject><ispartof>Molecular cell, 2009-09, Vol.35 (5), p.716-723</ispartof><rights>2009 Elsevier Inc.</rights><rights>2009 Elsevier Inc. All rights reserved. 2009</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c527t-a617281cb21b42364471595f10d9796ec767fb54460d5cb44da7a6e5a79784ab3</citedby><cites>FETCH-LOGICAL-c527t-a617281cb21b42364471595f10d9796ec767fb54460d5cb44da7a6e5a79784ab3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1097276509004754$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19748364$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shen, Xi</creatorcontrib><creatorcontrib>Do, Huong</creatorcontrib><creatorcontrib>Li, Yongjiang</creatorcontrib><creatorcontrib>Chung, Woo-Hyun</creatorcontrib><creatorcontrib>Tomasz, Maria</creatorcontrib><creatorcontrib>de Winter, Johan P.</creatorcontrib><creatorcontrib>Xia, Bing</creatorcontrib><creatorcontrib>Elledge, Stephen J.</creatorcontrib><creatorcontrib>Wang, Weidong</creatorcontrib><creatorcontrib>Li, Lei</creatorcontrib><title>Recruitment of Fanconi Anemia and Breast Cancer Proteins to DNA Damage Sites Is Differentially Governed by Replication</title><title>Molecular cell</title><addtitle>Mol Cell</addtitle><description>Fanconi anemia (FA) is characterized by cellular hypersensitivity to DNA crosslinking agents, but how the Fanconi pathway protects cells from DNA crosslinks and whether FA proteins act directly on crosslinks remain unclear. We developed a chromatin-IP-based strategy termed eChIP and detected association of multiple FA proteins with DNA crosslinks in vivo. Interdependence analyses revealed that crosslink-specific enrichment of various FA proteins is controlled by distinct mechanisms. BRCA-related FA proteins (BRCA2, FANCJ/BACH1, and FANCN/PALB2), but not FA core and I/D2 complexes, require replication for their crosslink association. FANCD2, but not FANCJ and FANCN, requires the FA core complex for its recruitment. FA core complex requires nucleotide excision repair proteins XPA and XPC for its association. Consistent with the distinct recruitment mechanism, recombination-independent crosslink repair was inversely affected in cells deficient of FANC-core versus BRCA-related FA proteins. Thus, FA proteins participate in distinct DNA damage response mechanisms governed by DNA replication status.</description><subject>Apoptosis Regulatory Proteins</subject><subject>Basic-Leucine Zipper Transcription Factors - genetics</subject><subject>Basic-Leucine Zipper Transcription Factors - metabolism</subject><subject>BRCA2 Protein - genetics</subject><subject>BRCA2 Protein - metabolism</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Cell Line, Tumor</subject><subject>Chromatin Immunoprecipitation - methods</subject><subject>Cross-Linking Reagents - pharmacology</subject><subject>DNA</subject><subject>DNA Damage</subject><subject>DNA Replication</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Fanconi Anemia Complementation Group D2 Protein - genetics</subject><subject>Fanconi Anemia Complementation Group D2 Protein - metabolism</subject><subject>Fanconi Anemia Complementation Group N Protein</subject><subject>Fanconi Anemia Complementation Group Proteins - genetics</subject><subject>Fanconi Anemia Complementation Group Proteins - metabolism</subject><subject>Female</subject><subject>Ficusin - pharmacology</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Mutation</subject><subject>Nuclear Proteins - genetics</subject><subject>Nuclear Proteins - metabolism</subject><subject>Plasmids - metabolism</subject><subject>Recombination, Genetic</subject><subject>Time Factors</subject><subject>Tumor Suppressor Proteins - genetics</subject><subject>Tumor Suppressor Proteins - metabolism</subject><subject>Xeroderma Pigmentosum Group A Protein - metabolism</subject><issn>1097-2765</issn><issn>1097-4164</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU1vEzEQhlcIREvhHyDkE7ds7Y0_1hekkNBSqaJVgbM1650tjnbtYDuR8u9xlYi2l55mpJl55515quojozWjTJ6v6ymMFse6oVTXVNZ0zl9Vp4xqNeNM8tfHvFFSnFTvUlpTyrho9dvqhGnF27nkp9XuDm3cujyhzyQM5AK8Dd6RhcfJAQHfk68RIWWyLBWM5DaGjM4nkgNZ_ViQFUxwj-Sny5jIVSIrNwwYi5qDcdyTy7DD6LEn3Z7c4WZ0FrIL_n31ZoAx4YdjPKt-X3z7tfw-u765vFourmdWNCrPQDLVtMx2Det4UwxzxYQWA6O9VlqiVVINneBc0l7YjvMeFEgUoLRqOXTzs-rLQXez7SbsbfEVYTSb6CaIexPAmecV7_6Y-7AzjRKtkrIIfD4KxPB3iymbyaXy9RE8hm0yUkmuKVelkR8abQwpRRz-L2HUPAAza3MAZh6AGSpNAVbGPj01-Dh0JPR4AZY37RxGk6zDgqJ3EW02fXAvb_gHhrmqZg</recordid><startdate>20090911</startdate><enddate>20090911</enddate><creator>Shen, Xi</creator><creator>Do, Huong</creator><creator>Li, Yongjiang</creator><creator>Chung, Woo-Hyun</creator><creator>Tomasz, Maria</creator><creator>de Winter, Johan P.</creator><creator>Xia, Bing</creator><creator>Elledge, Stephen J.</creator><creator>Wang, Weidong</creator><creator>Li, Lei</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</scope><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>5PM</scope></search><sort><creationdate>20090911</creationdate><title>Recruitment of Fanconi Anemia and Breast Cancer Proteins to DNA Damage Sites Is Differentially Governed by Replication</title><author>Shen, Xi ; Do, Huong ; Li, Yongjiang ; Chung, Woo-Hyun ; Tomasz, Maria ; de Winter, Johan P. ; Xia, Bing ; Elledge, Stephen J. ; Wang, Weidong ; Li, Lei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c527t-a617281cb21b42364471595f10d9796ec767fb54460d5cb44da7a6e5a79784ab3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Apoptosis Regulatory Proteins</topic><topic>Basic-Leucine Zipper Transcription Factors - genetics</topic><topic>Basic-Leucine Zipper Transcription Factors - metabolism</topic><topic>BRCA2 Protein - genetics</topic><topic>BRCA2 Protein - metabolism</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>Cell Line, Tumor</topic><topic>Chromatin Immunoprecipitation - methods</topic><topic>Cross-Linking Reagents - pharmacology</topic><topic>DNA</topic><topic>DNA Damage</topic><topic>DNA Replication</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Fanconi Anemia Complementation Group D2 Protein - genetics</topic><topic>Fanconi Anemia Complementation Group D2 Protein - metabolism</topic><topic>Fanconi Anemia Complementation Group N Protein</topic><topic>Fanconi Anemia Complementation Group Proteins - genetics</topic><topic>Fanconi Anemia Complementation Group Proteins - metabolism</topic><topic>Female</topic><topic>Ficusin - pharmacology</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>Mutation</topic><topic>Nuclear Proteins - genetics</topic><topic>Nuclear Proteins - metabolism</topic><topic>Plasmids - metabolism</topic><topic>Recombination, Genetic</topic><topic>Time Factors</topic><topic>Tumor Suppressor Proteins - genetics</topic><topic>Tumor Suppressor Proteins - metabolism</topic><topic>Xeroderma Pigmentosum Group A Protein - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shen, Xi</creatorcontrib><creatorcontrib>Do, Huong</creatorcontrib><creatorcontrib>Li, Yongjiang</creatorcontrib><creatorcontrib>Chung, Woo-Hyun</creatorcontrib><creatorcontrib>Tomasz, Maria</creatorcontrib><creatorcontrib>de Winter, Johan P.</creatorcontrib><creatorcontrib>Xia, Bing</creatorcontrib><creatorcontrib>Elledge, Stephen J.</creatorcontrib><creatorcontrib>Wang, Weidong</creatorcontrib><creatorcontrib>Li, Lei</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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>PubMed Central (Full Participant titles)</collection><jtitle>Molecular cell</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shen, Xi</au><au>Do, Huong</au><au>Li, Yongjiang</au><au>Chung, Woo-Hyun</au><au>Tomasz, Maria</au><au>de Winter, Johan P.</au><au>Xia, Bing</au><au>Elledge, Stephen J.</au><au>Wang, Weidong</au><au>Li, Lei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Recruitment of Fanconi Anemia and Breast Cancer Proteins to DNA Damage Sites Is Differentially Governed by Replication</atitle><jtitle>Molecular cell</jtitle><addtitle>Mol Cell</addtitle><date>2009-09-11</date><risdate>2009</risdate><volume>35</volume><issue>5</issue><spage>716</spage><epage>723</epage><pages>716-723</pages><issn>1097-2765</issn><eissn>1097-4164</eissn><abstract>Fanconi anemia (FA) is characterized by cellular hypersensitivity to DNA crosslinking agents, but how the Fanconi pathway protects cells from DNA crosslinks and whether FA proteins act directly on crosslinks remain unclear. We developed a chromatin-IP-based strategy termed eChIP and detected association of multiple FA proteins with DNA crosslinks in vivo. Interdependence analyses revealed that crosslink-specific enrichment of various FA proteins is controlled by distinct mechanisms. BRCA-related FA proteins (BRCA2, FANCJ/BACH1, and FANCN/PALB2), but not FA core and I/D2 complexes, require replication for their crosslink association. FANCD2, but not FANCJ and FANCN, requires the FA core complex for its recruitment. FA core complex requires nucleotide excision repair proteins XPA and XPC for its association. Consistent with the distinct recruitment mechanism, recombination-independent crosslink repair was inversely affected in cells deficient of FANC-core versus BRCA-related FA proteins. Thus, FA proteins participate in distinct DNA damage response mechanisms governed by DNA replication status.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>19748364</pmid><doi>10.1016/j.molcel.2009.06.034</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Cell Press Free Archives; Elsevier ScienceDirect Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Free Full-Text Journals in Chemistry |
| subjects | Apoptosis Regulatory Proteins Basic-Leucine Zipper Transcription Factors - genetics Basic-Leucine Zipper Transcription Factors - metabolism BRCA2 Protein - genetics BRCA2 Protein - metabolism Breast Neoplasms - genetics Breast Neoplasms - metabolism Breast Neoplasms - pathology Cell Line, Tumor Chromatin Immunoprecipitation - methods Cross-Linking Reagents - pharmacology DNA DNA Damage DNA Replication DNA-Binding Proteins - metabolism Fanconi Anemia Complementation Group D2 Protein - genetics Fanconi Anemia Complementation Group D2 Protein - metabolism Fanconi Anemia Complementation Group N Protein Fanconi Anemia Complementation Group Proteins - genetics Fanconi Anemia Complementation Group Proteins - metabolism Female Ficusin - pharmacology Gene Expression Regulation, Neoplastic Humans Mutation Nuclear Proteins - genetics Nuclear Proteins - metabolism Plasmids - metabolism Recombination, Genetic Time Factors Tumor Suppressor Proteins - genetics Tumor Suppressor Proteins - metabolism Xeroderma Pigmentosum Group A Protein - metabolism |
| title | Recruitment of Fanconi Anemia and Breast Cancer Proteins to DNA Damage Sites Is Differentially Governed by Replication |
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