Dyson P, Schrempf H
Institut für Genetik und Mikrobiologie, Universität München, Federal Republic of Germany.
J Bacteriol. 1987 Oct;169(10):4796-803. doi: 10.1128/jb.169.10.4796-4803.1987.
Streptomyces lividans 66 exhibits genetic instability, involving sequential loss of resistance to chloramphenicol (Cams) and subsequent mutation of argG. Associated with this instability is the amplification of a 5.7-kilobase (kb) amplified DNA sequence (ADS). We have characterized a second, independent pathway of genetic instability, involving sequential loss of resistance to tetracycline (Tets) followed by mutation in nitrogen assimilation (Ntr). We detected DNA amplification in many of these mutant strains, as well as other reiterations coresident with the 5.7-kb ADS in Cams Arg mutants. However, in contrast to the 5.7-kb ADS, none of the novel elements were observed to amplify at high frequency. The mutation of argG is due to a deletion, one endpoint of which is defined by the 5.7-kb ADS. This amplification derives from a structure, the tandemly duplicated amplifiable unit of DNA (AUD), present in the wild-type genome. We found that progenitor strains containing just a single-copy AUD failed to reproducibly generate amplification of this element in Cams argG mutants, and DNA deletion endpoints proximal to the element were found to be unspecific. These results suggest that a duplicated AUD structure is required for high-frequency amplification and that this reiteration can subsequently buffer the extent of deletion formation in the relevant chromosomal region.
变铅青链霉菌66表现出遗传不稳定性,包括对氯霉素(Cams)抗性的相继丧失以及随后argG的突变。与这种不稳定性相关的是一个5.7千碱基(kb)的扩增DNA序列(ADS)的扩增。我们已经鉴定出另一条独立的遗传不稳定途径,包括对四环素(Tets)抗性的相继丧失,随后是氮同化(Ntr)的突变。我们在许多这些突变菌株中检测到DNA扩增,以及与Cams Arg突变体中5.7-kb ADS共存的其他重复序列。然而,与5.7-kb ADS不同,没有观察到任何新元件以高频扩增。argG的突变是由于一个缺失,其一个端点由5.7-kb ADS定义。这种扩增源自野生型基因组中存在的一种结构,即串联重复的可扩增DNA单元(AUD)。我们发现仅含有单拷贝AUD的祖代菌株在Cams argG突变体中未能可重复地产生该元件的扩增,并且在该元件附近的DNA缺失端点是不特异的。这些结果表明,高频扩增需要一个重复的AUD结构,并且这种重复随后可以缓冲相关染色体区域中缺失形成的程度。