Koraimann G, Koraimann C, Koronakis V, Schlager S, Högenauer G
Institut für Mikrobiologie, Karl-Franzens-Universität Graz, Austria.
Mol Microbiol. 1991 Jan;5(1):77-87. doi: 10.1111/j.1365-2958.1991.tb01828.x.
The finP gene of plasmid R1 is located between the genes traM and traJ, partially overlapping the first few nucleotides of the latter. It codes for a repressor of the conjugation system. The product of this gene is a small RNA of 72 nucleotides and, because it is transcribed from the opposite DNA strand, it is complementary to the 5' non-translated sequences, the ribosome-binding site, and the first two codons of traJ mRNA. The finP transcript is present in much higher concentrations in R1 than in R1-19 containing cells, the latter being a derepressed mutant of the former. A synthetic finP gene expressed from a synthetic lambda PL promoter markedly reduced the conjugation frequency of pDB12, a multicopy derivative of R1-19. Mutagenesis of finP showed that only finP loop II mutants have lost the ability to repress conjugation of R1-19 in trans. They are also the only ones which derepress conjugal DNA transfer of R1, probably by competing for the finO product, a molecule needed as corepressor for maximal activity. Mutations interrupting potential open reading frames of finP do not abolish finP repressor activity. Hence finP acts as an antisense RNA blocking the expression of the traJ gene by interacting with traJ mRNA through loop II.
质粒R1的finP基因位于traM基因和traJ基因之间,部分与后者的前几个核苷酸重叠。它编码一种接合系统的阻遏物。该基因的产物是一种72个核苷酸的小RNA,由于它是从相反的DNA链转录而来,所以它与traJ mRNA的5'非翻译序列、核糖体结合位点以及前两个密码子互补。finP转录本在R1中的浓度比在含有R1 - 19的细胞中高得多,后者是前者的去阻遏突变体。从合成的λPL启动子表达的合成finP基因显著降低了pDB12(R1 - 19的多拷贝衍生物)的接合频率。finP的诱变表明,只有finP环II突变体失去了反式抑制R1 - 19接合的能力。它们也是唯一能使R1的接合性DNA转移去阻遏的突变体,可能是通过与finO产物竞争,finO产物是最大活性所需的作为共阻遏物的分子。中断finP潜在开放阅读框的突变不会消除finP阻遏物活性。因此,finP作为一种反义RNA,通过环II与traJ mRNA相互作用来阻断traJ基因的表达。