FKBP25 participates in DNA double-strand break repair.
Identifieur interne : 000120 ( Main/Exploration ); précédent : 000119; suivant : 000121FKBP25 participates in DNA double-strand break repair.
Auteurs : David Dilworth [Canada] ; Fade Gong [États-Unis] ; Kyle Miller [États-Unis] ; Christopher J. Nelson [Canada]Source :
- Biochemistry and cell biology = Biochimie et biologie cellulaire [ 1208-6002 ] ; 2020.
Descripteurs français
- KwdFr :
- MESH :
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Tacrolimus Binding Proteins.
- Cell Proliferation, DNA Breaks, Double-Stranded, DNA Repair, Fluorescent Antibody Technique, Humans, Tumor Cells, Cultured.
Abstract
FK506-binding proteins (FKBPs) alter the conformation of proteins via cis-trans isomerization of prolyl-peptide bonds. While this activity can be demonstrated in vitro, the intractability of detecting prolyl isomerization events in cells has limited our understanding of the biological processes regulated by FKBPs. Here we report that FKBP25 is an active participant in the repair of DNA double-strand breaks (DSBs). FKBP25 influences DSB repair pathway choice by promoting homologous recombination (HR) and suppressing single-strand annealing (SSA). Consistent with this observation, cells depleted of FKBP25 form fewer Rad51 repair foci in response to etoposide and ionizing radiation, and they are reliant on the SSA repair factor Rad52 for viability. We find that FKBP25's catalytic activity is required for promoting DNA repair, which is the first description of a biological function for this enzyme activity. Consistent with the importance of the FKBP catalytic site in HR, rapamycin treatment also impairs homologous recombination, and this effect is at least in part independent of mTor. Taken together these results identify FKBP25 as a component of the DNA DSB repair pathway.
DOI: 10.1139/bcb-2018-0328
PubMed: 30620620
PubMed Central: PMC7457334
Affiliations:
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Nelson</name><affiliation wicri:level="1"><nlm:affiliation>The Department of Biochemistry & Microbiology, University of Victoria, Victoria, BC V8W 3P6, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>The Department of Biochemistry & Microbiology, University of Victoria, Victoria, BC V8W 3P6</wicri:regionArea><wicri:noRegion>BC V8W 3P6</wicri:noRegion></affiliation></author></analytic><series><title level="j">Biochemistry and cell biology = Biochimie et biologie cellulaire</title><idno type="eISSN">1208-6002</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cell Proliferation (MeSH)</term><term>DNA Breaks, Double-Stranded (MeSH)</term><term>DNA Repair (MeSH)</term><term>Fluorescent Antibody Technique (MeSH)</term><term>Humans (MeSH)</term><term>Tacrolimus Binding Proteins (metabolism)</term><term>Tumor Cells, Cultured (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Cassures double-brin de l'ADN (MeSH)</term><term>Cellules cancéreuses en culture (MeSH)</term><term>Humains (MeSH)</term><term>Prolifération cellulaire (MeSH)</term><term>Protéines de liaison au tacrolimus (métabolisme)</term><term>Réparation de l'ADN (MeSH)</term><term>Technique d'immunofluorescence (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Tacrolimus Binding Proteins</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Protéines de liaison au tacrolimus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Proliferation</term><term>DNA Breaks, Double-Stranded</term><term>DNA Repair</term><term>Fluorescent Antibody Technique</term><term>Humans</term><term>Tumor Cells, Cultured</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Cassures double-brin de l'ADN</term><term>Cellules cancéreuses en culture</term><term>Humains</term><term>Prolifération cellulaire</term><term>Réparation de l'ADN</term><term>Technique d'immunofluorescence</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">FK506-binding proteins (FKBPs) alter the conformation of proteins via <i>cis-trans</i> isomerization of prolyl-peptide bonds. While this activity can be demonstrated in vitro, the intractability of detecting prolyl isomerization events in cells has limited our understanding of the biological processes regulated by FKBPs. Here we report that FKBP25 is an active participant in the repair of DNA double-strand breaks (DSBs). FKBP25 influences DSB repair pathway choice by promoting homologous recombination (HR) and suppressing single-strand annealing (SSA). Consistent with this observation, cells depleted of FKBP25 form fewer Rad51 repair foci in response to etoposide and ionizing radiation, and they are reliant on the SSA repair factor Rad52 for viability. We find that FKBP25's catalytic activity is required for promoting DNA repair, which is the first description of a biological function for this enzyme activity. Consistent with the importance of the FKBP catalytic site in HR, rapamycin treatment also impairs homologous recombination, and this effect is at least in part independent of mTor. Taken together these results identify FKBP25 as a component of the DNA DSB repair pathway.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30620620</PMID><DateCompleted><Year>2020</Year><Month>04</Month><Day>08</Day></DateCompleted><DateRevised><Year>2020</Year><Month>09</Month><Day>01</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1208-6002</ISSN><JournalIssue CitedMedium="Internet"><Volume>98</Volume><Issue>1</Issue><PubDate><Year>2020</Year><Month>02</Month></PubDate></JournalIssue><Title>Biochemistry and cell biology = Biochimie et biologie cellulaire</Title><ISOAbbreviation>Biochem Cell Biol</ISOAbbreviation></Journal><ArticleTitle>FKBP25 participates in DNA double-strand break repair.</ArticleTitle><Pagination><MedlinePgn>42-49</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1139/bcb-2018-0328</ELocationID><Abstract><AbstractText>FK506-binding proteins (FKBPs) alter the conformation of proteins via <i>cis-trans</i> isomerization of prolyl-peptide bonds. While this activity can be demonstrated in vitro, the intractability of detecting prolyl isomerization events in cells has limited our understanding of the biological processes regulated by FKBPs. Here we report that FKBP25 is an active participant in the repair of DNA double-strand breaks (DSBs). FKBP25 influences DSB repair pathway choice by promoting homologous recombination (HR) and suppressing single-strand annealing (SSA). Consistent with this observation, cells depleted of FKBP25 form fewer Rad51 repair foci in response to etoposide and ionizing radiation, and they are reliant on the SSA repair factor Rad52 for viability. We find that FKBP25's catalytic activity is required for promoting DNA repair, which is the first description of a biological function for this enzyme activity. Consistent with the importance of the FKBP catalytic site in HR, rapamycin treatment also impairs homologous recombination, and this effect is at least in part independent of mTor. Taken together these results identify FKBP25 as a component of the DNA DSB repair pathway.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Dilworth</LastName><ForeName>David</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>The Department of Biochemistry & Microbiology, University of Victoria, Victoria, BC V8W 3P6, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gong</LastName><ForeName>Fade</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Institute for Cellular and Molecular Biology, Department of Molecular Biosciences, University of Texas at Austin, 2506 Speedway Stop A5000, Austin, TX 78712 USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Miller</LastName><ForeName>Kyle</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Institute for Cellular and Molecular Biology, Department of Molecular Biosciences, University of Texas at Austin, 2506 Speedway Stop A5000, Austin, TX 78712 USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nelson</LastName><ForeName>Christopher J</ForeName><Initials>CJ</Initials><AffiliationInfo><Affiliation>The Department of Biochemistry & Microbiology, University of Victoria, Victoria, BC V8W 3P6, Canada.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 CA198279</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 CA201268</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate 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Nelson</name></country><country name="États-Unis"><region name="Texas"><name sortKey="Gong, Fade" sort="Gong, Fade" uniqKey="Gong F" first="Fade" last="Gong">Fade Gong</name></region><name sortKey="Miller, Kyle" sort="Miller, Kyle" uniqKey="Miller K" first="Kyle" last="Miller">Kyle Miller</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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|texte= FKBP25 participates in DNA double-strand break repair.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i -Sk "pubmed:30620620" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd \
| NlmPubMed2Wicri -a RapamycinFungusV1
| This area was generated with Dilib version V0.6.38. |  |