质粒
生物
突变体
基因
核糖核酸
滚动圆复制
复制的起源
分子生物学
遗传学
DNA复制
作者
Sarah K. Highlander,Richard P. Novick
出处
期刊:Plasmid
[Elsevier]
日期:1990-01-01
卷期号:23 (1): 1-15
被引量:15
标识
DOI:10.1016/0147-619x(90)90039-f
摘要
Plasmid pT181 is a small multicopy plasmid from Staphylococcus aureus that belongs to incompatibility group 3 and expresses two distinct types of incompatibility, Inc3A and Inc3B. Inc3A incompatibility is expressed by the primary replication control determinant, copA, which specifies two small transcripts, RNA I and RNA II, that jointly inhibit the synthesis of the rate-limiting initiator protein, RepC. Inc3B incompatibility is expressed by the leading strand replication origin and is due to competition for RepC. The copA region from each of 11 different pT181 copy number mutants was cloned onto the pT181-compatible vector, pE194, and tested for its ability to inhibit the replication of pT181 and its copy number mutants. The pT181 replication origin was also cloned and tested for its ability to inhibit the replication of the same plasmids. In general copA mutations that alter the production or sequence of RNA I and RNA II greatly reduced or completely eliminated Inc3A activity. Unlike the wild-type, all of the copy mutants were resistant to Inc3B inhibition. The separately cloned wild-type copA and ori regions each reduced the copy number of pT181 in proportion to their gene dosage, but neither blocked replication completely. It is proposed that the cloned Inc determinants cause incompatibility by interfering with the plasmid's copy correction mechanism; this interference destabilizes the plasmid even under conditions where its average copy number is not greatly reduced.
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