The iron-sulfur helicase DDX11 promotes the generation of single-stranded DNA for CHK1 activation.
Identifieur interne : 000018 ( Main/Exploration ); précédent : 000017; suivant : 000019The iron-sulfur helicase DDX11 promotes the generation of single-stranded DNA for CHK1 activation.
Auteurs : Anna K. Simon [Suisse] ; Sandra Kummer [Suisse] ; Sebastian Wild [Suisse] ; Aleksandra Lezaja [Suisse] ; Federico Teloni [Suisse] ; Stanislaw K. Jozwiakowski [Suisse] ; Matthias Altmeyer [Suisse] ; Kerstin Gari [Suisse]Source :
- Life science alliance [ 2575-1077 ] ; 2020.
Abstract
The iron-sulfur (FeS) cluster helicase DDX11 is associated with a human disorder termed Warsaw Breakage Syndrome. Interestingly, one disease-associated mutation affects the highly conserved arginine-263 in the FeS cluster-binding motif. Here, we demonstrate that the FeS cluster in DDX11 is required for DNA binding, ATP hydrolysis, and DNA helicase activity, and that arginine-263 affects FeS cluster binding, most likely because of its positive charge. We further show that DDX11 interacts with the replication factors DNA polymerase delta and WDHD1. In vitro, DDX11 can remove DNA obstacles ahead of Pol δ in an ATPase- and FeS domain-dependent manner, and hence generate single-stranded DNA. Accordingly, depletion of DDX11 causes reduced levels of single-stranded DNA, a reduction of chromatin-bound replication protein A, and impaired CHK1 phosphorylation at serine-345. Taken together, we propose that DDX11 plays a role in dismantling secondary structures during DNA replication, thereby promoting CHK1 activation.
DOI: 10.26508/lsa.201900547
PubMed: 32071282
PubMed Central: PMC7032568
Affiliations:
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Simon</name><affiliation wicri:level="4"><nlm:affiliation>Institute of Molecular Cancer Research, University of Zurich, Zurich, Switzerland.</nlm:affiliation><country xml:lang="fr">Suisse</country><wicri:regionArea>Institute of Molecular Cancer Research, University of Zurich, Zurich</wicri:regionArea><orgName type="university">Université de Zurich</orgName><placeName><settlement type="city">Zurich</settlement><region nuts="3" type="region">Canton de Zurich</region></placeName></affiliation></author><author><name sortKey="Kummer, Sandra" sort="Kummer, Sandra" uniqKey="Kummer S" first="Sandra" last="Kummer">Sandra Kummer</name><affiliation wicri:level="4"><nlm:affiliation>Institute of Molecular Cancer Research, University of Zurich, Zurich, Switzerland.</nlm:affiliation><country xml:lang="fr">Suisse</country><wicri:regionArea>Institute of Molecular Cancer Research, University of Zurich, Zurich</wicri:regionArea><orgName type="university">Université de Zurich</orgName><placeName><settlement type="city">Zurich</settlement><region nuts="3" type="region">Canton de Zurich</region></placeName></affiliation></author><author><name sortKey="Wild, Sebastian" sort="Wild, Sebastian" uniqKey="Wild S" first="Sebastian" last="Wild">Sebastian Wild</name><affiliation wicri:level="4"><nlm:affiliation>Institute of Molecular Cancer Research, University of Zurich, Zurich, Switzerland.</nlm:affiliation><country xml:lang="fr">Suisse</country><wicri:regionArea>Institute of Molecular Cancer Research, University of Zurich, Zurich</wicri:regionArea><orgName type="university">Université de Zurich</orgName><placeName><settlement type="city">Zurich</settlement><region nuts="3" type="region">Canton de Zurich</region></placeName></affiliation></author><author><name sortKey="Lezaja, Aleksandra" sort="Lezaja, Aleksandra" uniqKey="Lezaja A" first="Aleksandra" last="Lezaja">Aleksandra Lezaja</name><affiliation wicri:level="4"><nlm:affiliation>Department of Molecular Mechanisms of Disease, University of Zurich, Zurich, Switzerland.</nlm:affiliation><country xml:lang="fr">Suisse</country><wicri:regionArea>Department of Molecular Mechanisms of Disease, University of Zurich, Zurich</wicri:regionArea><orgName type="university">Université de Zurich</orgName><placeName><settlement type="city">Zurich</settlement><region nuts="3" type="region">Canton de Zurich</region></placeName></affiliation></author><author><name sortKey="Teloni, Federico" sort="Teloni, Federico" uniqKey="Teloni F" first="Federico" last="Teloni">Federico Teloni</name><affiliation wicri:level="4"><nlm:affiliation>Department of Molecular Mechanisms of Disease, University of Zurich, Zurich, Switzerland.</nlm:affiliation><country xml:lang="fr">Suisse</country><wicri:regionArea>Department of Molecular Mechanisms of Disease, University of Zurich, Zurich</wicri:regionArea><orgName type="university">Université de Zurich</orgName><placeName><settlement type="city">Zurich</settlement><region nuts="3" type="region">Canton de Zurich</region></placeName></affiliation></author><author><name sortKey="Jozwiakowski, Stanislaw K" sort="Jozwiakowski, Stanislaw K" uniqKey="Jozwiakowski S" first="Stanislaw K" last="Jozwiakowski">Stanislaw K. Jozwiakowski</name><affiliation wicri:level="4"><nlm:affiliation>Institute of Molecular Cancer Research, University of Zurich, Zurich, Switzerland.</nlm:affiliation><country xml:lang="fr">Suisse</country><wicri:regionArea>Institute of Molecular Cancer Research, University of Zurich, Zurich</wicri:regionArea><orgName type="university">Université de Zurich</orgName><placeName><settlement type="city">Zurich</settlement><region nuts="3" type="region">Canton de Zurich</region></placeName></affiliation></author><author><name sortKey="Altmeyer, Matthias" sort="Altmeyer, Matthias" uniqKey="Altmeyer M" first="Matthias" last="Altmeyer">Matthias Altmeyer</name><affiliation wicri:level="4"><nlm:affiliation>Department of Molecular Mechanisms of Disease, University of Zurich, Zurich, Switzerland.</nlm:affiliation><country xml:lang="fr">Suisse</country><wicri:regionArea>Department of Molecular Mechanisms of Disease, University of Zurich, Zurich</wicri:regionArea><orgName type="university">Université de Zurich</orgName><placeName><settlement type="city">Zurich</settlement><region nuts="3" type="region">Canton de Zurich</region></placeName></affiliation></author><author><name sortKey="Gari, Kerstin" sort="Gari, Kerstin" uniqKey="Gari K" first="Kerstin" last="Gari">Kerstin Gari</name><affiliation wicri:level="4"><nlm:affiliation>Institute of Molecular Cancer Research, University of Zurich, Zurich, Switzerland gari@imcr.uzh.ch.</nlm:affiliation><country wicri:rule="url">Suisse</country><wicri:regionArea>Institute of Molecular Cancer Research, University of Zurich, Zurich</wicri:regionArea><orgName type="university">Université de Zurich</orgName><placeName><settlement type="city">Zurich</settlement><region nuts="3" type="region">Canton de Zurich</region></placeName></affiliation></author></analytic><series><title level="j">Life science alliance</title><idno type="eISSN">2575-1077</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The iron-sulfur (FeS) cluster helicase DDX11 is associated with a human disorder termed Warsaw Breakage Syndrome. Interestingly, one disease-associated mutation affects the highly conserved arginine-263 in the FeS cluster-binding motif. Here, we demonstrate that the FeS cluster in DDX11 is required for DNA binding, ATP hydrolysis, and DNA helicase activity, and that arginine-263 affects FeS cluster binding, most likely because of its positive charge. We further show that DDX11 interacts with the replication factors DNA polymerase delta and WDHD1. In vitro, DDX11 can remove DNA obstacles ahead of Pol δ in an ATPase- and FeS domain-dependent manner, and hence generate single-stranded DNA. Accordingly, depletion of DDX11 causes reduced levels of single-stranded DNA, a reduction of chromatin-bound replication protein A, and impaired CHK1 phosphorylation at serine-345. Taken together, we propose that DDX11 plays a role in dismantling secondary structures during DNA replication, thereby promoting CHK1 activation.</div></front></TEI><pubmed><MedlineCitation Status="In-Process" Owner="NLM"><PMID Version="1">32071282</PMID><DateRevised><Year>2020</Year><Month>06</Month><Day>26</Day></DateRevised><Article PubModel="Electronic-Print"><Journal><ISSN IssnType="Electronic">2575-1077</ISSN><JournalIssue CitedMedium="Internet"><Volume>3</Volume><Issue>3</Issue><PubDate><Year>2020</Year><Month>03</Month></PubDate></JournalIssue><Title>Life science alliance</Title><ISOAbbreviation>Life Sci Alliance</ISOAbbreviation></Journal><ArticleTitle>The iron-sulfur helicase DDX11 promotes the generation of single-stranded DNA for CHK1 activation.</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">e201900547</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.26508/lsa.201900547</ELocationID><Abstract><AbstractText>The iron-sulfur (FeS) cluster helicase DDX11 is associated with a human disorder termed Warsaw Breakage Syndrome. Interestingly, one disease-associated mutation affects the highly conserved arginine-263 in the FeS cluster-binding motif. Here, we demonstrate that the FeS cluster in DDX11 is required for DNA binding, ATP hydrolysis, and DNA helicase activity, and that arginine-263 affects FeS cluster binding, most likely because of its positive charge. We further show that DDX11 interacts with the replication factors DNA polymerase delta and WDHD1. In vitro, DDX11 can remove DNA obstacles ahead of Pol δ in an ATPase- and FeS domain-dependent manner, and hence generate single-stranded DNA. Accordingly, depletion of DDX11 causes reduced levels of single-stranded DNA, a reduction of chromatin-bound replication protein A, and impaired CHK1 phosphorylation at serine-345. Taken together, we propose that DDX11 plays a role in dismantling secondary structures during DNA replication, thereby promoting CHK1 activation.</AbstractText><CopyrightInformation>© 2020 Simon et al.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Simon</LastName><ForeName>Anna K</ForeName><Initials>AK</Initials><AffiliationInfo><Affiliation>Institute of Molecular Cancer Research, University of Zurich, Zurich, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kummer</LastName><ForeName>Sandra</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Institute of Molecular Cancer Research, University of Zurich, Zurich, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wild</LastName><ForeName>Sebastian</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Institute of Molecular Cancer Research, University of Zurich, Zurich, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lezaja</LastName><ForeName>Aleksandra</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Molecular Mechanisms of Disease, University of Zurich, Zurich, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Teloni</LastName><ForeName>Federico</ForeName><Initials>F</Initials><Identifier Source="ORCID">0000-0003-0953-8010</Identifier><AffiliationInfo><Affiliation>Department of Molecular Mechanisms of Disease, University of Zurich, Zurich, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jozwiakowski</LastName><ForeName>Stanislaw K</ForeName><Initials>SK</Initials><Identifier Source="ORCID">0000-0002-0553-3530</Identifier><AffiliationInfo><Affiliation>Institute of Molecular Cancer Research, University of Zurich, Zurich, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Altmeyer</LastName><ForeName>Matthias</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Molecular Mechanisms of Disease, University of Zurich, Zurich, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gari</LastName><ForeName>Kerstin</ForeName><Initials>K</Initials><Identifier Source="ORCID">0000-0003-1276-8941</Identifier><AffiliationInfo><Affiliation>Institute of Molecular Cancer Research, University of Zurich, Zurich, Switzerland gari@imcr.uzh.ch.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>02</Month><Day>18</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Life Sci 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Simon</name></region><name sortKey="Altmeyer, Matthias" sort="Altmeyer, Matthias" uniqKey="Altmeyer M" first="Matthias" last="Altmeyer">Matthias Altmeyer</name><name sortKey="Gari, Kerstin" sort="Gari, Kerstin" uniqKey="Gari K" first="Kerstin" last="Gari">Kerstin Gari</name><name sortKey="Jozwiakowski, Stanislaw K" sort="Jozwiakowski, Stanislaw K" uniqKey="Jozwiakowski S" first="Stanislaw K" last="Jozwiakowski">Stanislaw K. Jozwiakowski</name><name sortKey="Kummer, Sandra" sort="Kummer, Sandra" uniqKey="Kummer S" first="Sandra" last="Kummer">Sandra Kummer</name><name sortKey="Lezaja, Aleksandra" sort="Lezaja, Aleksandra" uniqKey="Lezaja A" first="Aleksandra" last="Lezaja">Aleksandra Lezaja</name><name sortKey="Teloni, Federico" sort="Teloni, Federico" uniqKey="Teloni F" first="Federico" last="Teloni">Federico Teloni</name><name sortKey="Wild, Sebastian" sort="Wild, Sebastian" uniqKey="Wild S" first="Sebastian" last="Wild">Sebastian Wild</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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|area= IronSulferCluV1
|flux= Main
|étape= Exploration
|type= RBID
|clé= pubmed:32071282
|texte= The iron-sulfur helicase DDX11 promotes the generation of single-stranded DNA for CHK1 activation.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i -Sk "pubmed:32071282" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd \
| NlmPubMed2Wicri -a IronSulferCluV1
| This area was generated with Dilib version V0.6.38. |  |