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Fork Cleavage-Religation Cycle and Active Transcription Mediate Replication Restart after Fork Stalling at Co-transcriptional R-Loops
N. Chappidi, Z. Nascakova, B. Boleslavska, R. Zellweger, E. Isik, M. Andrs, S. Menon, J. Dobrovolna, C. Balbo Pogliano, J. Matos, A. Porro, M. Lopes, P. Janscak,
Language English Country United States
Document type Journal Article, Research Support, Non-U.S. Gov't
NLK
Cell Press Free Archives
from 1997-12-01 to 1 year ago
Free Medical Journals
from 1997 to 1 year ago
Free Medical Journals
from 1997 to 1 year ago
Open Access Digital Library
from 1997-12-01
Elsevier Open Access Journals
from 1997-12-01 to 2023-06-15
Elsevier Open Archive Journals
from 1997-12-01 to 1 year ago
- MeSH
- Rad52 DNA Repair and Recombination Protein metabolism MeSH
- DNA-Binding Proteins metabolism MeSH
- DNA Ligases metabolism MeSH
- DNA Polymerase III metabolism MeSH
- Endodeoxyribonucleases metabolism MeSH
- Endonucleases genetics metabolism MeSH
- Transcription, Genetic genetics MeSH
- HeLa Cells MeSH
- RecQ Helicases metabolism physiology MeSH
- Humans MeSH
- Cell Line, Tumor MeSH
- R-Loop Structures genetics physiology MeSH
- Rad51 Recombinase genetics metabolism physiology MeSH
- DNA Replication genetics physiology MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
Formation of co-transcriptional R-loops underlies replication fork stalling upon head-on transcription-replication encounters. Here, we demonstrate that RAD51-dependent replication fork reversal induced by R-loops is followed by the restart of semiconservative DNA replication mediated by RECQ1 and RECQ5 helicases, MUS81/EME1 endonuclease, RAD52 strand-annealing factor, the DNA ligase IV (LIG4)/XRCC4 complex, and the non-catalytic subunit of DNA polymerase δ, POLD3. RECQ5 disrupts RAD51 filaments assembled on stalled forks after RECQ1-mediated reverse branch migration, preventing a new round of fork reversal and facilitating fork cleavage by MUS81/EME1. MUS81-dependent DNA breaks accumulate in cells lacking RAD52 or LIG4 upon induction of R-loop formation, suggesting that RAD52 acts in concert with LIG4/XRCC4 to catalyze fork religation, thereby mediating replication restart. The resumption of DNA synthesis after R-loop-associated fork stalling also requires active transcription, the restoration of which depends on MUS81, RAD52, LIG4, and the transcription elongation factor ELL. These findings provide mechanistic insights into transcription-replication conflict resolution.
References provided by Crossref.org
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