THE NATURE OF X-RAY-INDUCED MUTATIONS AFTER RECOVERY IN EXCISION REPAIR-DEFICIENT (MUS-201) DROSOPHILA FEMALES

被引:8
作者
EEKEN, JCJ [1 ]
VREEKEN, C [1 ]
DEJONG, AWM [1 ]
PASTINK, A [1 ]
机构
[1] INTERUNIV RES INST RADIOPATHOL & RADIAT PROTECT, JA COHEN INST, LEIDEN, NETHERLANDS
来源
MUTATION RESEARCH | 1991年 / 247卷 / 01期
关键词
GENETIC AND MOLECULAR ANALYSIS; X-RAY-INDUCED MUTATIONS; REPAIR-DEFICIENT DROSOPHILA;
D O I
10.1016/0027-5107(91)90040-U
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
This paper describes the genetic analysis of X-ray-induced mutations at several visible loci (yellow, white, Notch, vermilion and forked) located on the X-chromosome of Drosophila melanogaster after recovery in excision repair-deficient condition (mus-201). A total of 118 mutations observed in 83636 F1 females were analyzed. The white mutations in particular have been investigated at the molecular level. The results show that: (1) the frequency of recovered whole-body mutations is similar or slightly lower in repair-deficient than in repair-proficient condition (respectively 1.5 x 10(-4)/locus/15 Gy and 2.3 x 10(-4)/locus/15 Gy); (2) the frequency of observed mosaic mutations is significantly higher in the repair-deficient condition than in the proficient condition (respectively 2.7 x 10(-4)/locus/15 Gy); (3) the analysis of F2 male lethal mutations and the cytological analysis of the recovered mutations in the excision repair-deficient condition indicate a decrease in mutations associated with gross chromosomal aberrations (including multilocus deletions); (4) at the molecular level, the spectrum of recovered intragenic mutations is similar after excision-deficient and -proficient repair. These results indicate that excision repair is involved in X-ray-induced DNA damage that is repaired efficiently in the normal repair condition, but bypassed in the excision repair-deficient condition, leading to mosaic mutations. In addition, lesions that apparently cannot be bypassed by DNA replication lead to a decrease in the fraction of mutations due to gross chromosomal aberrations among the whole-body mutations.
引用
收藏
页码:129 / 140
页数:12
相关论文
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