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Am J Physiol Cell Physiol 283: C878-C884, 2002. First published May 22, 2002; doi:10.1152/ajpcell.00107.2002
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Vol. 283, Issue 3, C878-C884, September 2002

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

Dorothea M. Peters1, Jacob B. Griffin1, J. Steven Stanley2, Mary M. Beck3, and Janos Zempleni1,4

Departments of 1 Nutritional Science and Dietetics, 3 Animal Science, and 4 Biochemistry, University of Nebraska at Lincoln, Lincoln, Nebraska 68583; and 2 Arkansas Children's Hospital Research Institute, Little Rock, Arkansas 72202

Biotin in breakdown products of biotinylated carboxylases serves as substrate for biotinylation of histones by biotinidase. Here we determined whether biotinylation of histones might play a role in repair of damaged DNA and in apoptosis. Jurkat cells were exposed to UV light to induce DNA damage. Abundance of thymine dimers increased about three times in response to UV exposure, consistent with DNA damage. Biotin-containing carboxylases were degraded in response to UV exposure, as judged by Western blot analysis and carboxylase activities. Mitochondrial integrity decreased in response to UV exposure (as judged by confocal microscopy), facilitating the release of breakdown products of carboxylases from mitochondria. Biotinylation of histones increased in response to UV exposure; biotinylation of histones did not occur specifically at sites of newly repaired DNA. UV exposure triggered apoptosis, as judged by caspase-3 activity and analysis by confocal microscopy. In summary, this study provided evidence that increased biotinylation of histones in DNA-damaged cells might either be a side product of carboxylase degradation or a step during apoptosis.

apoptosis; biotin; carboxylases; DNA damage


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