Schubert I, Rieger R
Hum Genet. 1981;57(2):119-30. doi: 10.1007/BF00282006.
The inter- and intrachromosomal distribution patterns of SCEs obtained with or without mutagen treatment are reviewed and compared, with each other as to their relation to heterochromatin and with the distribution patterns of chromatid aberrations that occurred either "spontaneously" in chromosomes of repair-defective human syndromes or after treatment with the mutagens (BrdU, ethylalcohol, DMBA, TMBA, maleic hydrazide, MMS, MMC). The conclusions are: No general rule is detectable for nonrandom involvement of heterochromatin in spontaneous SCEs. Mutagen-induced SCEs show the same or very similar distribution patterns as the spontaneous ones and are in no case as preferentially located as chromatid aberrations (which involve mainly the junctions between eu- and heterochromatin or other special regions). Therefore, a specific mutagen sensitivity of heterochromatin-aberrations does not exist (or is less pronounced) for SCEs. This supports the inference that different mechanisms underlie the origins of the two phenomena.
本文回顾并比较了经或未经诱变处理所获得的姐妹染色单体交换（SCE）在染色体间和染色体内的分布模式，比较了它们彼此之间与异染色质的关系，以及与在修复缺陷型人类综合征染色体中“自发”出现的或经诱变剂（5-溴脱氧尿嘧啶核苷、乙醇、二甲基苯并蒽、四甲基苯并蒽、马来酰肼、甲基磺酸甲酯、丝裂霉素C）处理后出现的染色单体畸变的分布模式。结论如下：在自发SCE中，未发现异染色质非随机参与的一般规律。诱变剂诱导的SCE显示出与自发SCE相同或非常相似的分布模式，且在任何情况下都不像染色单体畸变那样优先定位（染色单体畸变主要涉及常染色质与异染色质之间的连接处或其他特殊区域）。因此，对于SCE而言，不存在（或不太明显）异染色质畸变的特定诱变敏感性。这支持了两种现象起源背后存在不同机制的推断。
