Other
12 Authors
- Liu J,
- You MJ,
- Castillo A,
- Wu L,
- Komatsu Y,
- Su D,
- Wu X,
- Wang B,
- Atkinson E,
- Schlacher K,
- Paul A,
- Xu S
| First Author | Xu S | Year | 2017 |
| Journal | Genes Dev | Volume | 31 |
| Issue | 14 | Pages | 1469-1482 |
| PubMed ID | 28860160 | Mgi Jnum | J:245949 |
| Mgi Id | MGI:5917513 | Doi | 10.1101/gad.299172.117 |
| Citation | Xu S, et al. (2017) Abro1 maintains genome stability and limits replication stress by protecting replication fork stability. Genes Dev 31(14):1469-1482 |
| abstractText | Protection of the stalled replication fork is crucial for responding to replication stress and minimizing its impact on chromosome instability, thus preventing diseases, including cancer. We found a new component, Abro1, in the protection of stalled replication fork integrity. Abro1 deficiency results in increased chromosome instability, and Abro1-null mice are tumor-prone. We show that Abro1 protects stalled replication fork stability by inhibiting DNA2 nuclease/WRN helicase-mediated degradation of stalled forks. Depletion of RAD51 prevents the DNA2/WRN-dependent degradation of stalled forks in Abro1-deficient cells. This mechanism is distinct from the BRCA2-dependent fork protection pathway, in which stable RAD51 filament formation prevents MRE11-dependent degradation of the newly synthesized DNA at stalled forks. Thus, our data reveal a new aspect of regulated protection of stalled replication forks that involves Abro1. |
