Cellular senescence, an irreversible growth arrest triggered by a variety of 
stressors, plays important roles in normal physiology and tumor suppression, but 
accumulation of senescent cells with age contributes to the functional decline 
of tissues. Senescent cells undergo dramatic alterations to their chromatin 
landscape that affect genome accessibility and their transcriptional program. 
These include the loss of DNA-nuclear lamina interactions, the distension of 
centromeres, and changes in chromatin composition that can lead to the 
activation of retrotransposons. Here we discuss these findings, as well as 
recent advances in microscopy and genomics that have revealed the importance of 
the higher-order spatial organization of the genome in defining and maintaining 
the senescent state.