The chromatin assembly factor 1 promotes Rad51-dependent template switches at replication forks by counteracting D-loop disassembly by the RecQ-type helicase Rqh1.
At blocked replication forks, homologous recombination mediates the nascent strands to switch template in order to ensure replication restart, but faulty template switches underlie genome rearrangements in cancer cells and genomic disorders. Recombination occurs within DNA packaged into chromatin th...
Saved in:
Main Authors: | Violena Pietrobon, Karine Fréon, Julien Hardy, Audrey Costes, Ismail Iraqui, Françoise Ochsenbein, Sarah A E Lambert |
---|---|
Format: | article |
Language: | EN |
Published: |
Public Library of Science (PLoS)
2014
|
Subjects: | |
Online Access: | https://doaj.org/article/ef4b215e1b334916b42dcb87135b1af6 |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Similar Items
-
HERC2 inactivation abrogates nucleolar localization of RecQ helicases BLM and WRN
by: Mingzhang Zhu, et al.
Published: (2021) -
A guanine-flipping and sequestration mechanism for G-quadruplex unwinding by RecQ helicases
by: Andrew F. Voter, et al.
Published: (2018) -
The structural and functional characterization of human RecQ4 reveals insights into its helicase mechanism
by: Sebastian Kaiser, et al.
Published: (2017) -
Elucidation of DNA Repair Function of PfBlm and Potentiation of Artemisinin Action by a Small-Molecule Inhibitor of RecQ Helicase
by: Niranjan Suthram, et al.
Published: (2020) -
Non-enzymatic roles of human RAD51 at stalled replication forks
by: Jennifer M. Mason, et al.
Published: (2019)