Recruitment of damaged DNA to the nuclear matrix in hamster cells following ultraviolet irradiation.
We examined the relationship between the nuclear matrix and DNA in the dihydrofolate reductase domain following irradiation of Chinese hamster cells with UV light. The fraction of matrix-bound DNA increased in transcribed and non-transcribed regions during a 3 h period after irradiation. However, no increase was observed with excision repair-deficient cells mutant for the ERCC1 gene. The major UV-induced lesion, the cyclobutane pyrimidine dimer, increased in frequency in the matrix-bound DNA 1 h after irradiation, in both transcribed and non-transcribed regions, but decreased subsequently. This phenomenon was also lacking in excision repair-deficient cells. These data demonstrate that recruitment of lesion-containing DNA to the nuclear matrix occurs following UV irradiation and suggest that this recruitment is dependent upon nucleotide excision repair. This is consistent with the concept of a 'repair factory' residing on the nuclear matrix at which excision repair occurs.
Koehler
D R
DR
Department of Biological Sciences, Stanford University, CA 94305-5020, USA.
Hanawalt
P C
PC
D000818:Animals; D016466:CHO Cells; D002451:Cell Compartmentation; D006224:Cricetinae; D004249:DNA Damage; D004260:DNA Repair; D015530:Nuclear Matrix / Q000378:metabolism*; D013347:Subcellular Fractions; D013762:Tetrahydrofolate Dehydrogenase / Q000378:metabolism; D014466:Ultraviolet Rays / Q000009:adverse effects*
D013762:Tetrahydrofolate Dehydrogenase