Vertebrate CTF18 and DDX11 essential function in cohesion is bypassed by preventing WAPL-mediated cohesin release
The alternative PCNA loader containing CTF18-DCC1-CTF8 facilitates sister chromatid cohesion (SCC) by poorly defined mechanisms. Here we found that in DT40 cells, CTF18 acts complementarily with the Warsaw breakage syndrome DDX11 helicase in mediating SCC and proliferation. We uncover that the letha...
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| Veröffentlicht in: | Genes & development 2021-10, Vol.35 (19-20), p.1368-1382 |
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| container_title | Genes & development |
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| creator | Kawasumi, Ryotaro Abe, Takuya Psakhye, Ivan Miyata, Keiji Hirota, Kouji Branzei, Dana |
| description | The alternative PCNA loader containing CTF18-DCC1-CTF8 facilitates sister chromatid cohesion (SCC) by poorly defined mechanisms. Here we found that in DT40 cells, CTF18 acts complementarily with the Warsaw breakage syndrome DDX11 helicase in mediating SCC and proliferation. We uncover that the lethality and cohesion defects of
mutants are associated with reduced levels of chromatin-bound cohesin and rescued by depletion of WAPL, a cohesin-removal factor. On the contrary, high levels of
acetyltransferases that acetylate cohesin to establish SCC do not rescue
phenotypes. Notably, the tight proximity of sister centromeres and increased anaphase bridges characteristic of WAPL-depleted cells are abrogated by loss of both
and
The results reveal that vertebrate CTF18 and DDX11 collaborate to provide sufficient amounts of chromatin-loaded cohesin available for SCC generation in the presence of WAPL-mediated cohesin-unloading activity. This process modulates chromosome structure and is essential for cellular proliferation in vertebrates. |
| doi_str_mv | 10.1101/gad.348581.121 |
| format | Article |
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mutants are associated with reduced levels of chromatin-bound cohesin and rescued by depletion of WAPL, a cohesin-removal factor. On the contrary, high levels of
acetyltransferases that acetylate cohesin to establish SCC do not rescue
phenotypes. Notably, the tight proximity of sister centromeres and increased anaphase bridges characteristic of WAPL-depleted cells are abrogated by loss of both
and
The results reveal that vertebrate CTF18 and DDX11 collaborate to provide sufficient amounts of chromatin-loaded cohesin available for SCC generation in the presence of WAPL-mediated cohesin-unloading activity. This process modulates chromosome structure and is essential for cellular proliferation in vertebrates.</description><identifier>ISSN: 0890-9369</identifier><identifier>EISSN: 1549-5477</identifier><identifier>DOI: 10.1101/gad.348581.121</identifier><identifier>PMID: 34503989</identifier><language>eng</language><publisher>United States: Cold Spring Harbor Laboratory Press</publisher><subject>Animals ; Cell Cycle Proteins - genetics ; Chromatids - genetics ; Chromosomal Proteins, Non-Histone - genetics ; Cohesins ; Research Paper ; Vertebrates - genetics</subject><ispartof>Genes & development, 2021-10, Vol.35 (19-20), p.1368-1382</ispartof><rights>2021 Kawasumi et al.; Published by Cold Spring Harbor Laboratory Press.</rights><rights>2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c456t-8e5c7c522983688fc9b74e3ea4a974259256ea24f144f3d90cd75ff1e1dac703</citedby><cites>FETCH-LOGICAL-c456t-8e5c7c522983688fc9b74e3ea4a974259256ea24f144f3d90cd75ff1e1dac703</cites><orcidid>0000-0002-0544-4888 ; 0000-0003-3877-133X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8494208/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8494208/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34503989$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kawasumi, Ryotaro</creatorcontrib><creatorcontrib>Abe, Takuya</creatorcontrib><creatorcontrib>Psakhye, Ivan</creatorcontrib><creatorcontrib>Miyata, Keiji</creatorcontrib><creatorcontrib>Hirota, Kouji</creatorcontrib><creatorcontrib>Branzei, Dana</creatorcontrib><title>Vertebrate CTF18 and DDX11 essential function in cohesion is bypassed by preventing WAPL-mediated cohesin release</title><title>Genes & development</title><addtitle>Genes Dev</addtitle><description>The alternative PCNA loader containing CTF18-DCC1-CTF8 facilitates sister chromatid cohesion (SCC) by poorly defined mechanisms. Here we found that in DT40 cells, CTF18 acts complementarily with the Warsaw breakage syndrome DDX11 helicase in mediating SCC and proliferation. We uncover that the lethality and cohesion defects of
mutants are associated with reduced levels of chromatin-bound cohesin and rescued by depletion of WAPL, a cohesin-removal factor. On the contrary, high levels of
acetyltransferases that acetylate cohesin to establish SCC do not rescue
phenotypes. Notably, the tight proximity of sister centromeres and increased anaphase bridges characteristic of WAPL-depleted cells are abrogated by loss of both
and
The results reveal that vertebrate CTF18 and DDX11 collaborate to provide sufficient amounts of chromatin-loaded cohesin available for SCC generation in the presence of WAPL-mediated cohesin-unloading activity. This process modulates chromosome structure and is essential for cellular proliferation in vertebrates.</description><subject>Animals</subject><subject>Cell Cycle Proteins - genetics</subject><subject>Chromatids - genetics</subject><subject>Chromosomal Proteins, Non-Histone - genetics</subject><subject>Cohesins</subject><subject>Research Paper</subject><subject>Vertebrates - genetics</subject><issn>0890-9369</issn><issn>1549-5477</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkU1rGzEQhkVpSJyPa49Fx17W1ayklXQpGOejBUNyMEluQtbOOlvWWltaG_LvI8duaE4a0DPvvPAQ8g3YGIDBz6Wrx1xoqWEMJXwhI5DCFFIo9ZWMmDasMLwyZ-Q8pb-MsYpV1Sk540IybrQZkc0jxgEX0Q1Ip_Nb0NSFml5fPwNQTAnD0LqONtvgh7YPtA3U9y-Y3udEF69rl6E6D3QdcbfHw5I-TR5mxQrrNqfWx4VAI3boEl6Sk8Z1Ca-O7wWZ397Mp7-L2f3dn-lkVnghq6HQKL3ysiyN5pXWjTcLJZCjE84oUUpTygpdKRoQouG1Yb5WsmkAoXZeMX5Bfh1i19tFruJzteg6u47tysVX27vWfv4J7Ytd9jurhREl0zngxzEg9pstpsGu2uSx61zAfptsKRUYUILzjI4PqI99ShGbjzPA7F6TzZrsQZPNmvLC9__LfeD_vPA37XSPcw</recordid><startdate>20211001</startdate><enddate>20211001</enddate><creator>Kawasumi, Ryotaro</creator><creator>Abe, Takuya</creator><creator>Psakhye, Ivan</creator><creator>Miyata, Keiji</creator><creator>Hirota, Kouji</creator><creator>Branzei, Dana</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>5PM</scope><orcidid>https://orcid.org/0000-0002-0544-4888</orcidid><orcidid>https://orcid.org/0000-0003-3877-133X</orcidid></search><sort><creationdate>20211001</creationdate><title>Vertebrate CTF18 and DDX11 essential function in cohesion is bypassed by preventing WAPL-mediated cohesin release</title><author>Kawasumi, Ryotaro ; Abe, Takuya ; Psakhye, Ivan ; Miyata, Keiji ; Hirota, Kouji ; Branzei, Dana</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c456t-8e5c7c522983688fc9b74e3ea4a974259256ea24f144f3d90cd75ff1e1dac703</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Animals</topic><topic>Cell Cycle Proteins - genetics</topic><topic>Chromatids - genetics</topic><topic>Chromosomal Proteins, Non-Histone - genetics</topic><topic>Cohesins</topic><topic>Research Paper</topic><topic>Vertebrates - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kawasumi, Ryotaro</creatorcontrib><creatorcontrib>Abe, Takuya</creatorcontrib><creatorcontrib>Psakhye, Ivan</creatorcontrib><creatorcontrib>Miyata, Keiji</creatorcontrib><creatorcontrib>Hirota, Kouji</creatorcontrib><creatorcontrib>Branzei, Dana</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>PubMed Central (Full Participant titles)</collection><jtitle>Genes & development</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kawasumi, Ryotaro</au><au>Abe, Takuya</au><au>Psakhye, Ivan</au><au>Miyata, Keiji</au><au>Hirota, Kouji</au><au>Branzei, Dana</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Vertebrate CTF18 and DDX11 essential function in cohesion is bypassed by preventing WAPL-mediated cohesin release</atitle><jtitle>Genes & development</jtitle><addtitle>Genes Dev</addtitle><date>2021-10-01</date><risdate>2021</risdate><volume>35</volume><issue>19-20</issue><spage>1368</spage><epage>1382</epage><pages>1368-1382</pages><issn>0890-9369</issn><eissn>1549-5477</eissn><abstract>The alternative PCNA loader containing CTF18-DCC1-CTF8 facilitates sister chromatid cohesion (SCC) by poorly defined mechanisms. Here we found that in DT40 cells, CTF18 acts complementarily with the Warsaw breakage syndrome DDX11 helicase in mediating SCC and proliferation. We uncover that the lethality and cohesion defects of
mutants are associated with reduced levels of chromatin-bound cohesin and rescued by depletion of WAPL, a cohesin-removal factor. On the contrary, high levels of
acetyltransferases that acetylate cohesin to establish SCC do not rescue
phenotypes. Notably, the tight proximity of sister centromeres and increased anaphase bridges characteristic of WAPL-depleted cells are abrogated by loss of both
and
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| source | MEDLINE; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | Animals Cell Cycle Proteins - genetics Chromatids - genetics Chromosomal Proteins, Non-Histone - genetics Cohesins Research Paper Vertebrates - genetics |
| title | Vertebrate CTF18 and DDX11 essential function in cohesion is bypassed by preventing WAPL-mediated cohesin release |
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