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通过对宿主细胞进行UVB(313纳米)、UVA(334纳米、365纳米)和可见光(405纳米)照射,完整噬菌体中未诱导出非靶向突变。

Lack of induction of non-targeted mutations in intact bacteriophage by UVB (313 nm), UVA (334 nm, 365 nm) and visible (405 nm) irradiation of host cells.

作者信息

Tyrrell R M

出版信息

Mutat Res. 1984 Feb;139(2):45-9. doi: 10.1016/0165-7992(84)90101-5.

DOI:10.1016/0165-7992(84)90101-5
PMID:6229698
Abstract

Mutation to virulence has been measured in intact bacteriophage lambda 15 infected into host cells pre-treated with UVC (254 nm), UVB (313 nm), UVA (334 nm, 365 nm) or visible (405 nm) radiations. We have confirmed that UVC radiation leads to a large enhancement (maximum enhancement factor of 140 in wild-type) of the background spontaneous mutation frequency (non-targeted mutagenesis) and have further shown that this is at least partially dependent on excision repair (maximum enhancement factor of 14 in uvrA strain). In contrast, UVB (313 nm) radiation enhances the mutation frequency by less than a factor of 2. Longer wavelength UVA radiation (334 nm, 365 nm) actually reduces the mutation frequency to 25% of the background levels presumably by reducing the levels of viral replication occurring in the host cells. A visible wavelength (405 nm) has no effect on mutation frequency over the fluence range employed.

摘要

已对感染用UVC(254纳米)、UVB(313纳米)、UVA(334纳米、365纳米)或可见光(405纳米)辐射预处理过的宿主细胞的完整噬菌体λ15中的毒力突变进行了测定。我们已证实,UVC辐射会导致背景自发突变频率(非靶向诱变)大幅提高(野生型中的最大增强因子为140),并且进一步表明这至少部分依赖于切除修复(uvrA菌株中的最大增强因子为14)。相比之下,UVB(313纳米)辐射使突变频率提高不到2倍。波长更长的UVA辐射(334纳米、365纳米)实际上将突变频率降低至背景水平的25%,大概是通过降低宿主细胞中发生的病毒复制水平来实现的。在所采用的注量范围内,可见光波长(405纳米)对突变频率没有影响。

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