McKay Bruce C, Stubbert Lawton J, Fowler Casey C, Smith Jennifer M, Cardamore Robin A, Spronck Jennifer C
Centre for Cancer Therapeutics, Ottawa Regional Cancer Centre, Department of Radiology, University of Ottawa, 503 Smyth Road, Ottawa, ON, Canada K1C 5T5.
Proc Natl Acad Sci U S A. 2004 Apr 27;101(17):6582-6. doi: 10.1073/pnas.0308181101. Epub 2004 Apr 15.
UV light induces the expression of a wide variety of genes. At present, it is unclear how cells sense the extent of DNA damage and alter the expression of UV-induced genes appropriately. UV light induces DNA damage that blocks transcription, and the probability that a gene sustains transcription-blocking DNA damage is proportional to locus size and dose of UV light. Using colon carcinoma cells that express a temperature-sensitive variant of p53 and undergo p53-dependent apoptosis after UV irradiation, we found that the number of p53-induced genes identified by oligonucleotide microarray analysis decreased in a UV dose-dependent manner. This was associated with a statistically significant shift in the spectrum of p53-induced genes toward compact genes with fewer and smaller introns. Genes encoding proapoptotic proteins involved in the initiation of the mitochondrial apoptotic cascade were prominent among the compact p53 target genes, whereas genes encoding negative regulators of p53 and the mitochondrial apoptotic pathway were significantly larger. We propose that the shift in spectrum of UV-responsive gene expression caused by passive effects of UV lesions on transcription acts as a molecular dosimeter, ensuring the elimination of cells sustaining irreparable transcription-blocking DNA damage.
紫外线可诱导多种基因的表达。目前,尚不清楚细胞如何感知DNA损伤的程度并相应地改变紫外线诱导基因的表达。紫外线会诱导DNA损伤从而阻断转录,而一个基因遭受转录阻断性DNA损伤的概率与基因座大小和紫外线剂量成正比。利用表达p53温度敏感变体且在紫外线照射后会经历p53依赖性凋亡的结肠癌细胞,我们发现通过寡核苷酸微阵列分析鉴定出的p53诱导基因的数量呈紫外线剂量依赖性减少。这与p53诱导基因谱向内含子数量更少、更小的紧密基因发生统计学上的显著转变有关。在紧密的p53靶基因中,编码参与线粒体凋亡级联反应起始的促凋亡蛋白的基因较为突出,而编码p53和线粒体凋亡途径负调控因子的基因则明显更大。我们认为,紫外线损伤对转录的被动影响所导致的紫外线反应性基因表达谱的转变充当了一种分子剂量计,确保清除遭受无法修复的转录阻断性DNA损伤的细胞。