Replication fork plasticity upon genotoxic stress is modulated by nuclear architectural components by elusive mechanisms. Here the authors implicate Lamin A/C – best known for its structural support of nuclear periphery – in the control of replication fork restart throughout the nucleus, by supporting heterochromatin establishment and ADP ribosylation levels at replication factories.
- Veronica Cherdyntseva
- Joanna Paulson
- Massimo Lopes
