Lehmann A R, Kirk-Bell S, Mayne L
Cancer Res. 1979 Oct;39(10):4237-41.
Cells from patients with the hereditary disorder Cockayne's syndrome and from the sun-sensitive individual, 11961, are sensitive to the lethal effects of ultraviolet light (UV) but have no detectable defect in either excision- or postreplication repair after UV irradiation. In normal cells and in Cockayne heterozygotes, UV causes a depression in the rate of DNA-replicative synthesis followed by a recovery of normal rates 5 to 8 hr after irradiation. In Cockayne and 11961 cells, the initial depression in DNA synthesis is the same as that in normal cells, but no subsequent recovery is observed. The recovery of DNA synthesis in normal cells appears to be unaffected by fluorodeoxyuridine but inhibited by cycloheximide. This suggests a possible requirement for de novo protein synthesis, but there are a number of alternative interpretations of these data.
患有遗传性疾病科凯恩综合征的患者以及对阳光敏感的个体11961的细胞,对紫外线(UV)的致死效应敏感,但在紫外线照射后的切除修复或复制后修复中均未检测到缺陷。在正常细胞和科凯恩综合征杂合子中,紫外线会导致DNA复制合成速率下降,随后在照射后5至8小时恢复正常速率。在科凯恩综合征患者和11961细胞中,DNA合成的初始下降与正常细胞相同,但未观察到随后的恢复。正常细胞中DNA合成的恢复似乎不受氟脱氧尿苷的影响,但受环己酰亚胺抑制。这表明可能需要从头合成蛋白质,但对这些数据有许多其他解释。