Transfer RNA modification, temperature and DNA superhelicity have a common target in the regulatory network of the virulence of Shigella flexneri: the expression of the virF gene
| Autor: | Jérôme M. B. Durand, Björn Dagberg, Glenn R. Björk, Bernt Eric Uhlin |
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| Rok vydání: | 2000 |
| Předmět: |
DNA
Bacterial TRNA modification Transcription Genetic Virulence Factors Virulence Microbiology Shigella flexneri Bacterial Proteins RNA Transfer RNA Messenger RNA Processing Post-Transcriptional Molecular Biology Gene Regulator gene Genetics Regulation of gene expression Antigens Bacterial biology DNA Superhelical Structural gene Temperature Translation (biology) Gene Expression Regulation Bacterial biology.organism_classification Protein Biosynthesis Nucleic Acid Conformation |
| Zdroj: | Molecular microbiology. 35(4) |
| ISSN: | 0950-382X |
| Popis: | Full expression of the virulence genes of Shigella flexneri requires the presence of two modified nucleosides in the tRNA [queuosine, Q34, present in the wobble position (position 34) and 2-methylthio-N6-isopentenyladenosine (ms2i6A37, adjacent to and 3' of the anticodon)]. The synthesis of these two nucleosides depends on the products of the tgt and miaA genes respectively. We have shown that the intracellular concentration of the virulence-related transcriptional regulator VirF is reduced in the absence of either of these modified nucleosides. The intracellular concentration of VirF is correlated with the expression of the virulence genes. Overproduction of VirF in the tgt and the miaA mutants suppressed the less virulent (tgt) or the avirulent (miaA) phenotypes respectively, caused by the tRNA modification deficiency. This suggests that the primary result of undermodification of the tRNA is a poor translation of virF mRNA and not of any other mRNA whose product acts downstream of the action of VirF. Shigella showed no virulence phenotypes at 30 degrees C, but forced synthesis of VirF at 30 degrees C induced the virulence phenotype at this low temperature. In addition, removal of the known gene silencer H-NS by a mutation in its structural gene hns increased the synthesis of VirF at low temperature and thus induced a virulent phenotype at 30 degrees C. Conversely, decreased expression of VirF at 37 degrees C induced by the addition of novobiocin, a known inhibitor of gyrase, led to an avirulent phenotype. We conclude that tRNA modification, temperature and superhelicity have the same target - the expression of VirF - to influence the expression of the central regulatory gene virB and thereby the virulence of Shigella. These results further strengthen the suggestion that the concentration of VirF is the critical factor in the regulation of virulence in Shigella. In addition, they emphasize the role of the bacterial translational machinery in the regulation of the expression of virulence genes which appears here quantitatively as important as the well-established regulation on the transcriptional level. |
| Databáze: | OpenAIRE |
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