C17orf53 is identified as a novel gene involved in inter-strand crosslink repair
•C17orf53 promotes cell survival in response to ATR inhibition.•C17orf53-deficient cells show profound defect in response to ICL.•C17orf53 is a ssDNA-binding protein and directly interacts with RPA.•C17orf53 acts with MCM8/9 in DNA repair. Ataxia Telangiectasia and Rad3-Related kinase (ATR) is a mas...
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| Veröffentlicht in: | DNA repair 2020-11, Vol.95, p.102946-102946, Article 102946 |
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| container_title | DNA repair |
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| creator | Wang, Chao Chen, Zhen Su, Dan Tang, Mengfan Nie, Litong Zhang, Huimin Feng, Xu Wang, Rui Shen, Xi Srivastava, Mrinal McLaughlin, Megan E. Hart, Traver Li, Lei Chen, Junjie |
| description | •C17orf53 promotes cell survival in response to ATR inhibition.•C17orf53-deficient cells show profound defect in response to ICL.•C17orf53 is a ssDNA-binding protein and directly interacts with RPA.•C17orf53 acts with MCM8/9 in DNA repair.
Ataxia Telangiectasia and Rad3-Related kinase (ATR) is a master regulator of genome maintenance, and participates in DNA replication and various DNA repair pathways. In a genome-wide screen for ATR-dependent fitness genes, we identified a previously uncharacterized gene, C17orf53, whose loss led to hypersensitivity to ATR inhibition. C17orf53 is conserved in vertebrates and is required for efficient cell proliferation. Loss of C17orf53 slowed down DNA replication and led to pronounced interstrand crosslink (ICL) repair defect. We showed that C17orf53 is a ssDNA- and RPA-binding protein and both characteristics are important for its functions in the cell. In addition, using multiple omics methods, we found that C17orf53 works with MCM8/9 to promote cell survival in response to ICL lesions. Taken together, our data suggest that C17orf53 is a novel component involved in ICL repair pathway. |
| doi_str_mv | 10.1016/j.dnarep.2020.102946 |
| format | Article |
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Ataxia Telangiectasia and Rad3-Related kinase (ATR) is a master regulator of genome maintenance, and participates in DNA replication and various DNA repair pathways. In a genome-wide screen for ATR-dependent fitness genes, we identified a previously uncharacterized gene, C17orf53, whose loss led to hypersensitivity to ATR inhibition. C17orf53 is conserved in vertebrates and is required for efficient cell proliferation. Loss of C17orf53 slowed down DNA replication and led to pronounced interstrand crosslink (ICL) repair defect. We showed that C17orf53 is a ssDNA- and RPA-binding protein and both characteristics are important for its functions in the cell. In addition, using multiple omics methods, we found that C17orf53 works with MCM8/9 to promote cell survival in response to ICL lesions. Taken together, our data suggest that C17orf53 is a novel component involved in ICL repair pathway.</description><identifier>ISSN: 1568-7864</identifier><identifier>EISSN: 1568-7856</identifier><identifier>DOI: 10.1016/j.dnarep.2020.102946</identifier><identifier>PMID: 32853826</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Amino Acid Sequence ; C17orf53 ; Cell Survival ; DNA Adducts - metabolism ; DNA Repair ; DNA Replication ; DNA, Single-Stranded - metabolism ; DNA-Binding Proteins - chemistry ; DNA-Binding Proteins - metabolism ; DNA-Binding Proteins - physiology ; Genome-wide screen ; Humans ; ICL repair ; Minichromosome Maintenance Proteins - metabolism ; Replication Protein A - metabolism ; RPA-binding, HROB, MCM8IP ; Sequence Alignment ; ssDNA-binding</subject><ispartof>DNA repair, 2020-11, Vol.95, p.102946-102946, Article 102946</ispartof><rights>2020 The Author(s)</rights><rights>Copyright © 2020 The Author(s). Published by Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c463t-bfc01e614e3ad8de83473d94b5a8eb01f676e6ac3452749418102afae742873</citedby><cites>FETCH-LOGICAL-c463t-bfc01e614e3ad8de83473d94b5a8eb01f676e6ac3452749418102afae742873</cites><orcidid>0000-0002-9971-0111 ; 0000-0002-3191-9031 ; 0000-0002-1880-3341 ; 0000-0003-1603-7070</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.dnarep.2020.102946$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>230,314,780,784,885,3549,27923,27924,45994</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32853826$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Chao</creatorcontrib><creatorcontrib>Chen, Zhen</creatorcontrib><creatorcontrib>Su, Dan</creatorcontrib><creatorcontrib>Tang, Mengfan</creatorcontrib><creatorcontrib>Nie, Litong</creatorcontrib><creatorcontrib>Zhang, Huimin</creatorcontrib><creatorcontrib>Feng, Xu</creatorcontrib><creatorcontrib>Wang, Rui</creatorcontrib><creatorcontrib>Shen, Xi</creatorcontrib><creatorcontrib>Srivastava, Mrinal</creatorcontrib><creatorcontrib>McLaughlin, Megan E.</creatorcontrib><creatorcontrib>Hart, Traver</creatorcontrib><creatorcontrib>Li, Lei</creatorcontrib><creatorcontrib>Chen, Junjie</creatorcontrib><title>C17orf53 is identified as a novel gene involved in inter-strand crosslink repair</title><title>DNA repair</title><addtitle>DNA Repair (Amst)</addtitle><description>•C17orf53 promotes cell survival in response to ATR inhibition.•C17orf53-deficient cells show profound defect in response to ICL.•C17orf53 is a ssDNA-binding protein and directly interacts with RPA.•C17orf53 acts with MCM8/9 in DNA repair.
Ataxia Telangiectasia and Rad3-Related kinase (ATR) is a master regulator of genome maintenance, and participates in DNA replication and various DNA repair pathways. In a genome-wide screen for ATR-dependent fitness genes, we identified a previously uncharacterized gene, C17orf53, whose loss led to hypersensitivity to ATR inhibition. C17orf53 is conserved in vertebrates and is required for efficient cell proliferation. Loss of C17orf53 slowed down DNA replication and led to pronounced interstrand crosslink (ICL) repair defect. We showed that C17orf53 is a ssDNA- and RPA-binding protein and both characteristics are important for its functions in the cell. In addition, using multiple omics methods, we found that C17orf53 works with MCM8/9 to promote cell survival in response to ICL lesions. Taken together, our data suggest that C17orf53 is a novel component involved in ICL repair pathway.</description><subject>Amino Acid Sequence</subject><subject>C17orf53</subject><subject>Cell Survival</subject><subject>DNA Adducts - metabolism</subject><subject>DNA Repair</subject><subject>DNA Replication</subject><subject>DNA, Single-Stranded - metabolism</subject><subject>DNA-Binding Proteins - chemistry</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>DNA-Binding Proteins - physiology</subject><subject>Genome-wide screen</subject><subject>Humans</subject><subject>ICL repair</subject><subject>Minichromosome Maintenance Proteins - metabolism</subject><subject>Replication Protein A - metabolism</subject><subject>RPA-binding, HROB, MCM8IP</subject><subject>Sequence Alignment</subject><subject>ssDNA-binding</subject><issn>1568-7864</issn><issn>1568-7856</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9UU1LAzEQDaJYv_6BSI5etm422SS9CFL8AkFB7yFNZmvqNqnJdsF_b2pr1YswkCEz8-a9eQidknJISsIvZkPrdYTFsCqr1Vc1YnwHHZCay0LImu9uc84G6DClWVmSWnC-jwa0kjWVFT9AT2MiQmxqil3CzoLvXOPAYp2wxj700OIpeMDO96Htc8H5HB3EInVRe4tNDCm1zr_hzEW7eIz2Gt0mONm8R-j55vplfFc8PN7ej68eCsM47YpJY0oCnDCg2koLkjJB7YhNai1hUpKGCw5cG8rqSrARIzIr1I0GwSop6BG6XKMulpM5WJN5R92qRXRzHT9U0E79rXj3qqahV1n_iAuZAc43ADG8LyF1au6SgbbVHsIyqYpRyQWT9aqVrVu_pEZotmtIqVZWqJlaW6FWVqi1FXns7DfF7dD37X80QD5T7yCqZBx4A9ZFMJ2ywf2_4RMQjpzI</recordid><startdate>20201101</startdate><enddate>20201101</enddate><creator>Wang, Chao</creator><creator>Chen, Zhen</creator><creator>Su, Dan</creator><creator>Tang, Mengfan</creator><creator>Nie, Litong</creator><creator>Zhang, Huimin</creator><creator>Feng, Xu</creator><creator>Wang, Rui</creator><creator>Shen, Xi</creator><creator>Srivastava, Mrinal</creator><creator>McLaughlin, Megan E.</creator><creator>Hart, Traver</creator><creator>Li, Lei</creator><creator>Chen, Junjie</creator><general>Elsevier B.V</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><orcidid>https://orcid.org/0000-0002-9971-0111</orcidid><orcidid>https://orcid.org/0000-0002-3191-9031</orcidid><orcidid>https://orcid.org/0000-0002-1880-3341</orcidid><orcidid>https://orcid.org/0000-0003-1603-7070</orcidid></search><sort><creationdate>20201101</creationdate><title>C17orf53 is identified as a novel gene involved in inter-strand crosslink repair</title><author>Wang, Chao ; Chen, Zhen ; Su, Dan ; Tang, Mengfan ; Nie, Litong ; Zhang, Huimin ; Feng, Xu ; Wang, Rui ; Shen, Xi ; Srivastava, Mrinal ; McLaughlin, Megan E. ; Hart, Traver ; Li, Lei ; Chen, Junjie</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c463t-bfc01e614e3ad8de83473d94b5a8eb01f676e6ac3452749418102afae742873</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Amino Acid Sequence</topic><topic>C17orf53</topic><topic>Cell Survival</topic><topic>DNA Adducts - metabolism</topic><topic>DNA Repair</topic><topic>DNA Replication</topic><topic>DNA, Single-Stranded - metabolism</topic><topic>DNA-Binding Proteins - chemistry</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>DNA-Binding Proteins - physiology</topic><topic>Genome-wide screen</topic><topic>Humans</topic><topic>ICL repair</topic><topic>Minichromosome Maintenance Proteins - metabolism</topic><topic>Replication Protein A - metabolism</topic><topic>RPA-binding, HROB, MCM8IP</topic><topic>Sequence Alignment</topic><topic>ssDNA-binding</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Chao</creatorcontrib><creatorcontrib>Chen, Zhen</creatorcontrib><creatorcontrib>Su, Dan</creatorcontrib><creatorcontrib>Tang, Mengfan</creatorcontrib><creatorcontrib>Nie, Litong</creatorcontrib><creatorcontrib>Zhang, Huimin</creatorcontrib><creatorcontrib>Feng, Xu</creatorcontrib><creatorcontrib>Wang, Rui</creatorcontrib><creatorcontrib>Shen, Xi</creatorcontrib><creatorcontrib>Srivastava, Mrinal</creatorcontrib><creatorcontrib>McLaughlin, Megan E.</creatorcontrib><creatorcontrib>Hart, Traver</creatorcontrib><creatorcontrib>Li, Lei</creatorcontrib><creatorcontrib>Chen, Junjie</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>DNA repair</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Chao</au><au>Chen, Zhen</au><au>Su, Dan</au><au>Tang, Mengfan</au><au>Nie, Litong</au><au>Zhang, Huimin</au><au>Feng, Xu</au><au>Wang, Rui</au><au>Shen, Xi</au><au>Srivastava, Mrinal</au><au>McLaughlin, Megan E.</au><au>Hart, Traver</au><au>Li, Lei</au><au>Chen, Junjie</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>C17orf53 is identified as a novel gene involved in inter-strand crosslink repair</atitle><jtitle>DNA repair</jtitle><addtitle>DNA Repair (Amst)</addtitle><date>2020-11-01</date><risdate>2020</risdate><volume>95</volume><spage>102946</spage><epage>102946</epage><pages>102946-102946</pages><artnum>102946</artnum><issn>1568-7864</issn><eissn>1568-7856</eissn><abstract>•C17orf53 promotes cell survival in response to ATR inhibition.•C17orf53-deficient cells show profound defect in response to ICL.•C17orf53 is a ssDNA-binding protein and directly interacts with RPA.•C17orf53 acts with MCM8/9 in DNA repair.
Ataxia Telangiectasia and Rad3-Related kinase (ATR) is a master regulator of genome maintenance, and participates in DNA replication and various DNA repair pathways. In a genome-wide screen for ATR-dependent fitness genes, we identified a previously uncharacterized gene, C17orf53, whose loss led to hypersensitivity to ATR inhibition. C17orf53 is conserved in vertebrates and is required for efficient cell proliferation. Loss of C17orf53 slowed down DNA replication and led to pronounced interstrand crosslink (ICL) repair defect. We showed that C17orf53 is a ssDNA- and RPA-binding protein and both characteristics are important for its functions in the cell. In addition, using multiple omics methods, we found that C17orf53 works with MCM8/9 to promote cell survival in response to ICL lesions. Taken together, our data suggest that C17orf53 is a novel component involved in ICL repair pathway.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>32853826</pmid><doi>10.1016/j.dnarep.2020.102946</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0002-9971-0111</orcidid><orcidid>https://orcid.org/0000-0002-3191-9031</orcidid><orcidid>https://orcid.org/0000-0002-1880-3341</orcidid><orcidid>https://orcid.org/0000-0003-1603-7070</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | DNA repair, 2020-11, Vol.95, p.102946-102946, Article 102946 |
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| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | Amino Acid Sequence C17orf53 Cell Survival DNA Adducts - metabolism DNA Repair DNA Replication DNA, Single-Stranded - metabolism DNA-Binding Proteins - chemistry DNA-Binding Proteins - metabolism DNA-Binding Proteins - physiology Genome-wide screen Humans ICL repair Minichromosome Maintenance Proteins - metabolism Replication Protein A - metabolism RPA-binding, HROB, MCM8IP Sequence Alignment ssDNA-binding |
| title | C17orf53 is identified as a novel gene involved in inter-strand crosslink repair |
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