Mutagen-induced chromatid aberrations are not randomly distributed along the metaphase chromosomes. In the field bean (Vicia faba), defined late-replicating and transcriptionally inactive heterochromatic regions are preferentially involved. After exposure to the alkylating agent N-methyl-N-nitrosourea (MNU) (10(-3) M, 1 hour), 70% of all aberrations are clustered within 6 segments containing tandemly repeated FokI elements of 59 bp, which comprise approximately 10% of the genome. Using immuno-slot-blot analyses, we have studied the frequency of O6-methylguanine (O6-MeG), a mutagenic lesion important for aberration induction, in total genomic DNA as well as in FokI sequences of the field bean after exposure to MNU. In either case, similar numbers of adducts per nucleotide were found immediately after treatment as well as after 18 hours of recovery, when most adducts were removed and significant amounts of chromatid aberrations were detectable. Peculiarities of long FokI element arrays (e.g., formation of specific tertiary structures), resulting in error-prone recombination repair, rather than preferential formation or delayed repair of O6-MeG are apparently responsible for aberration clustering in these hot spot regions.

译文

诱变剂引起的染色单体畸变不是沿着中期染色体随机分布的。在田豆(Vicia faba)中,优先涉及定义的后期复制和无转录活性的异色区域。暴露于烷基化剂N-甲基-N-亚硝基脲(MNU)(10(-3)M,1小时)后,所有像差的70%聚集在6个片段中,这些片段包含串联重复的59 bp的FokI元素,约占59 bp。基因组的10%。使用免疫印迹分析,我们研究了O6-甲基鸟嘌呤(O6-MeG)的频率,这是一种对畸变诱导很重要的诱变病变,它暴露于MNU后总基因组DNA以及田豆的FokI序列中。在这两种情况下,当去除大多数加合物并检测到大量的染色单体畸变时,在治疗后以及恢复18小时后,发现每个核苷酸的加合物数量相似。长FokI元素阵列的特殊性(例如,形成特定的三级结构)导致容易出错的重组修复,而不是O6-MeG的优先形成或延迟修复,显然是这些热点区域中的像差聚类的原因。

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