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IDENTIFICATION OF A LARGE GENOMIC REGION IN UV‐IRRADIATED HUMAN CELLS WHICH HAS FEWER CYCLOBUTANE PYRIMIDINE DIMERS THAN MOST GENOMIC REGIONS
Author(s) -
Kantor G. J.,
DeissTolbert D. M.
Publication year - 1995
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/j.1751-1097.1995.tb05268.x
Subject(s) - pyrimidine dimer , cyclobutane , genomic dna , biology , dna , microbiology and biotechnology , genome , endonuclease , xeroderma pigmentosum , chemistry , gene , genetics , biochemistry , dna damage , ring (chemistry) , organic chemistry
— Size separation after UV‐endonuclease digestion of DNA from UV‐irradiated human cells using denaturing conditions fractionates the genome based on cyclobutane pyrimidine dimer content. We have examined the largest molecules available (50–80 kb; about 5% of the DNA) after fractionation and those of average size (5–15 kb) for content of some specific genes. We find that the largest molecules are not a representative sampling of the genome. Three contiguous genes located in a G+C‐rich isochore (tyrosine hydroxylase, insulin, insulin‐like growth factor II) have concentrations two to three times greater in the largest molecules. This shows that this genomic region has fewer pyrimidine dimers than most other genomic regions. In contrast, the p‐actin genomic region, which has a similar G+C content, has an equal concentration in both fractions as do the ß53 and ß‐globin genomic regions, which are A+T‐rich. These data show that DNA damage in the form of cyclobutane pyrimidine dimers occurs with different probabilities in specific isochores. Part of the reason may be the relative G + C content, but other factors must play a significant role. We also report that the transcriptionally inactive insulin region is repaired at the genome‐overall rate in normal cells and is not repaired in xeroderma pigmentosum complementation group C cells.