Fork restart: unloading FANCD2 to travel ahead

In this issue of Molecular Cell, Brunner et al. 1 Brunner A. Li Q. Fisicaro S. Kourtesakis A. Viiliäinen J. Johansson H.J. Pandey V. Mayank A.K. Lehtiö J. Wohlschlegel J.A. et al. FBXL12 degrades FANCD2 to regulate replication recovery and promote cancer cell survival under conditions of replication stress. Mol. Cell. 2023; 83: 3720-3739https://doi.org/10.1016/j.molcel.2023.07.026 Abstract Full Text Full Text PDF Google Scholar reveal that eliminating FANCD2 from stalled forks via FBXL12-mediated degradation enables cells to tolerate oncogene-induced replication stress, making FBXL12 a promising target for cancer treatment. In this issue of Molecular Cell, Brunner et al. 1 Brunner A. Li Q. Fisicaro S. Kourtesakis A. Viiliäinen J. Johansson H.J. Pandey V. Mayank A.K. Lehtiö J. Wohlschlegel J.A. et al. FBXL12 degrades FANCD2 to regulate replication recovery and promote cancer cell survival under conditions of replication stress. Mol. Cell. 2023; 83: 3720-3739https://doi.org/10.1016/j.molcel.2023.07.026 Abstract Full Text Full Text PDF Google Scholar reveal that eliminating FANCD2 from stalled forks via FBXL12-mediated degradation enables cells to tolerate oncogene-induced replication stress, making FBXL12 a promising target for cancer treatment. FBXL12 degrades FANCD2 to regulate replication recovery and promote cancer cell survival under conditions of replication stressBrunner et al.Molecular CellAugust 16, 2023In BriefThe Fanconi anemia pathway alleviates oncogene-induced replication stress. Brunner et al. report that the ubiquitin ligase SCFFBXL12 targets the key Fanconi anemia protein FANCD2 for proteasomal degradation. They demonstrate that this occurs in the vicinity of replication forks and is critical for replication recovery and survival under CDK-driven replication stress. Full-Text PDF Open Access