Heterochromatin-Driven Nuclear Softening Protects the Genome against Mechanical Stress-Induced Damage

Abstract

When tissues are stretched, cells respond via two distinct mechanosensory mechanisms to protect the genome from damage and maintain tissue homeostasis. First, rapid heterochromatin-mediated mechanosensing, independent of known cellular mechanosensors, drives calcium-dependent nuclear softening. If the mechanical stress persists, a second, tissue-level reorganization occurs, mediated by cell-cell contacts to redistribute mechanical energy to prevent force transmission to the nucleus.