Redox-sensitive alteration of replisome architecture safeguards genome integrity

Abstract

Metabolic regulation of genome stability Cells respond to metabolic fluctuations by adjusting the speed of DNA replication as a safeguard for genome stability. Somyajit et al. elucidate the cellular mechanisms that align replication fork dynamics with metabolic pathways (see the Perspective by Gómez-González and Aguilera). The elevation of reactive oxygen species (ROS) levels under metabolic stress dissociates a replication accelerator from the replisome and leads to replication slowdown, thus preventing replication stress. Studying this genome surveillance mechanism in cancer cells with elevated ROS levels and increased replication adaptability may provide opportunities to specifically target tumors. Science , this issue p. 797 ; see also p. 722