DNA double-strand breaks (DSBs) can induce chromosomal aberrations and 
carcinogenesis and their correct repair is crucial for genetic stability. The 
cellular response to DSBs depends on damage signaling including the 
phosphorylation of the histone H2AX (γH2AX). However, a lack of γH2AX formation 
in heterochromatin (HC) is generally observed after DNA damage induction. Here, 
we examine γH2AX and repair protein foci along linear ion tracks traversing 
heterochromatic regions in human or murine cells and find the DSBs and damage 
signal streaks bending around highly compacted DNA. Given the linear particle 
path, such bending indicates a relocation of damage from the initial induction 
site to the periphery of HC. Real-time imaging of the repair protein GFP-XRCC1 
confirms fast recruitment to heterochromatic lesions inside murine 
chromocenters. Using single-ion microirradiation to induce localized DSBs 
directly within chromocenters, we demonstrate that H2AX is early phosphorylated 
within HC, but the damage site is subsequently expelled from the center to the 
periphery of chromocenters within ∼ 20 min. While this process can occur in the 
absence of ATM kinase, the repair of DSBs bordering HC requires the protein. 
Finally, we describe a local decondensation of HC at the sites of ion hits, 
potentially allowing for DSB movement via physical forces.