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Updated: Aug 11, 2026

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Real-time Observation of the DNA Strand Exchange Reaction Mediated by Rad51
Published on: February 13, 2019
Nucleostemin promotes RAD51 filament assembly on double-stranded DNA to protect stalled replication forks
Chih-Chun Chang1, Siang-Sheng Tsai2, Chang-Le Chou3,4
1Institute of Biochemical Sciences, National Taiwan University, Taipei 106, Taiwan.
Nucleic Acids Research
|August 10, 2026
Summary
Nucleostemin (NS) stabilizes stalled DNA replication forks, preventing degradation. This discovery reveals a new mechanism protecting genome integrity during replication stress.
Area of Science:
- Molecular Biology
- Genetics
- Biochemistry
Background:
- Replication stress can stall DNA replication forks, leading to genome instability and double-stranded DNA breaks.
- Stalled forks can undergo reversal but remain susceptible to nucleolytic degradation.
Purpose of the Study:
- To identify factors that protect stalled and reversed replication forks.
- To elucidate the role of nucleostemin (NS) in maintaining genome integrity under replication stress.
Main Methods:
- Hydroxyurea treatment to induce replication stress.
- Immunofluorescence to detect RAD51 foci.
- Biochemical reconstitution assays.
- Single-molecule fluorescence resonance energy transfer (FRET).
Main Results:
- Nucleostemin (NS) rapidly accumulates at stalled replication forks.
- NS depletion prevents RAD51 foci formation and leads to MRE11-mediated DNA degradation.
- NS directly binds DNA and promotes RAD51 nucleoprotein filament assembly.
- The NS-RAD51 complex protects nascent DNA strands from nucleolytic attack.
Conclusions:
- Nucleostemin (NS) is a critical factor for stabilizing reversed replication forks.
- NS acts as a guardian of genome integrity by preventing fork degradation during replication stress.
- This study uncovers a novel mechanism of replication fork protection involving NS and RAD51.
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