Dutreix M, Bäckman A, Célérier J, Bagdasarian M M, Sommer S, Bailone A, Devoret R, Bagdasarian M
GEMC, Enzymologie, Centre National de la Recherche Scientifique, Gif-sur-Yvette, France.
Nucleic Acids Res. 1988 Nov 25;16(22):10669-79. doi: 10.1093/nar/16.22.10669.
PsiB protein of plasmid R6-5 inhibits the induction of the SOS pathway. The F sex factor also carries a psiB gene homologous to that of R6-5. Yet, it fails to inhibit SOS induction. In order to solve this difference, we characterized the psiB genes of R6-5 and F. We found that (i) the sequences of the two psiB genes share extensive homology the predicted amino acid sequences of the two proteins differing by 5 residues, (ii) the expression of R6-5 psiB is 4 times higher than F psiB gene, (iii) in plasmid R6-5, a Tn10 transposon upstream from the psiB gene enhances psiB expression. Hence, the F sex factor may be unable to prevent SOS induction for two non-exclusive reasons: (i) F PsiB protein, being slightly different from R6-5, may be less active, (ii) the level of synthesis of F PsiB protein may be insufficient to prevent SOS induction.
质粒R6 - 5的PsiB蛋白可抑制SOS途径的诱导。F性因子也携带一个与R6 - 5的psiB基因同源的基因。然而，它无法抑制SOS诱导。为了解决这一差异，我们对R6 - 5和F的psiB基因进行了表征。我们发现：（i）两个psiB基因的序列具有广泛的同源性，两种蛋白质的预测氨基酸序列仅相差5个残基；（ii）R6 - 5 psiB的表达比F psiB基因高4倍；（iii）在质粒R6 - 5中，psiB基因上游的一个Tn10转座子可增强psiB的表达。因此，F性因子可能由于两个并非相互排斥的原因而无法阻止SOS诱导：（i）F PsiB蛋白与R6 - 5略有不同，可能活性较低；（ii）F PsiB蛋白的合成水平可能不足以阻止SOS诱导。
