Exposure to UV light causes increased biotinylation of histones in Jurkat cells

Biotin in breakdown products ofbiotinylated carboxylases serves as substrate for biotinylation ofhistones by biotinidase. Here we determined whether biotinylation ofhistones might play a role in repair of damaged DNA and inapoptosis. Jurkat cells were exposed to UV light to induce DNAdamage. Abundance of thymine dimers increased about three times inresponse to UV exposure, consistent with DNA damage. Biotin-containingcarboxylases were degraded in response to UV exposure, as judged byWestern blot analysis and carboxylase activities. Mitochondrialintegrity decreased in response to UV exposure (as judged by confocalmicroscopy), facilitating the release of breakdown products ofcarboxylases from mitochondria. Biotinylation of histonesincreased in response to UV exposure; biotinylation of histones did notoccur specifically at sites of newly repaired DNA. UV exposuretriggered apoptosis, as judged by caspase-3 activity andanalysis by confocal microscopy. In summary, this study providedevidence that increased biotinylation of histones in DNA-damaged cellsmight either be a side product of carboxylase degradation or a stepduring apoptosis.