Yanase S, Hartman P S, Ito A, Ishii N
Department of Molecular Life Science, Tokai University School of Medicine, Isehara, Kanagawa 259-1193, Japan.
Mutat Res. 1999 May 3;426(1):31-9. doi: 10.1016/s0027-5107(99)00079-2.
Pre-exposure of wild-type Caenorhabditis elegans to oxygen conferred a protective effect against the lethality imposed by subsequent X-irradiation. In contrast, two mutants (rad-1 and rad-2) that are UV and ionizing radiation hypersensitive but not oxygen sensitive, did not exhibit this adaptive response. To explore the molecular basis of protection, the expression of several key genes was examined using Northern blot analyses to measure mRNA levels. In the wild-type, expression of the heat shock protein genes, hsp16-1 and hsp16-48, increased dramatically after incubation under high oxygen. Expression of two superoxide dismutase genes (sod-1 and sod-3) was relatively unaffected. Unlike the wild-type, the basal levels of these four genes were significantly lower in the rad-1 and rad-2 mutants under atmospheric conditions. These genes were partially induced in response to oxidative stress. These data suggest that at least a portion of the hypersensitive phenotype of rad-1 and rad-2 may be attributed to inappropriate gene expression.
将野生型秀丽隐杆线虫预先暴露于氧气中，可使其对随后的X射线照射所造成的致死性产生保护作用。相比之下，两个对紫外线和电离辐射敏感但对氧气不敏感的突变体（rad-1和rad-2）并未表现出这种适应性反应。为了探究保护作用的分子基础，使用Northern印迹分析检测了几个关键基因的表达，以测量mRNA水平。在野生型中，热休克蛋白基因hsp16-1和hsp16-48在高氧条件下孵育后表达显著增加。两个超氧化物歧化酶基因（sod-1和sod-3）的表达相对未受影响。与野生型不同，在大气条件下，rad-1和rad-2突变体中这四个基因的基础水平显著较低。这些基因在氧化应激反应中部分被诱导。这些数据表明，rad-1和rad-2的至少一部分超敏表型可能归因于不适当的基因表达。
