Prolonged treatment of proliferating mammalian cells with low doses of a histone deacetylase inhibitor, trichostatin A, specifically affects pericentric heterochromatin. Relocation of these regions towards the nuclear periphery and loss of HP1 proteins ensue after several divisions. Meanwhile, DNA methylation state and core centromeric markers are maintained. Subsequent defects in centromeric function arise in mitosis. Remarkably, removal of the drug rapidly reverses all these changes.
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