神经孢子菌us-16一个新的诱变敏感突变体

Hirokazu Inoue , Alice L. Schroeder
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引用次数: 6

摘要

一个新的基因,mus-16,是由Baker, Parish和Curtis(1984)的氮芥菜敏感神经孢子菌突变体确定的,该突变体在去除DNA-DNA和dna -蛋白质交联方面存在缺陷。该基因位于ca -1和lys-1之间的连锁组V的左臂上。突变体mu -16(JMB)对烷基化剂甲基磺酸甲酯(MMS)[剂量减少因子(drf) 8-10倍]、n -甲基-n′-硝基-n -亚硝基胍(drf) 5-6倍)、氨基酸组氨酸和药物羟基脲敏感。它对紫外线、γ辐射或丝裂霉素C (MMC)不敏感。它显示正常的自发突变率,但增加诱变的MMS。纯合子杂交是不育的,没有产孢的迹象。有丝分裂自发性染色体不稳定性增加。mus-6突变类似于神经孢子虫的几种非切除修复缺陷突变。其中一些在修复烷基化损伤时可能存在缺陷。MMC数据支持了真菌中MMC不能形成DNA-DNA交联的早期数据。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
A new mutagen-sensitive mutant in Neurospora, mus-16

A new gene, mus-16, is determined by the nitrogen mustard-sensitive Neurospora mutant of Baker, Parish and Curtis (1984) which is defective in the removal of DNA-DNA and DNA-protein crosslinks. This gene is on the left arm of linkage group V between caf-1 and lys-1. The mus-16(JMB) mutant is sensitive to the alkylating agents methyl methanesulfonate (MMS) [dose reduction factor (drf) 8–10 ×], N-methyl-N′-nitro-N-nitrosoguanidine (drf 5–6 ×), the amino acid histidine and the drug hydroxyurea. It is not sensitive to ultraviolet-light, γ-irradiation, or mitomycin C (MMC). It shows normal spontaneous mutation rates but increased induction of mutation by MMS. Homozygous crosses are barren, showing no signs of sporulation. Mitotic spontaneous chromosome instability is increased. The mus-6 mutation is similar to several non-excision repair-defective mutants in Neurospora. Some of these may be defective in repair of alkylation damage. The MMC data supports earlier data that in fungi MMC is incapable of forming DNA-DNA crosslinks.

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