RESUMO
The rpsO-pnp operon encodes ribosomal protein S15 and polynucleotide phosphorylase, a major 3'-5' exoribonuclease involved in mRNA decay in Escherichia coli The gene for the SraG small RNA is located between the coding regions of the rpsO and pnp genes, and it is transcribed in the opposite direction relative to the two genes. No function has been assigned to SraG. Multiple levels of post-transcriptional regulation have been demonstrated for the rpsO-pnp operon. Here we show that SraG is a new factor affecting pnp expression. SraG overexpression results in a reduction of pnp expression and a destabilization of pnp mRNA; in contrast, inhibition of SraG transcription results in a higher level of the pnp transcript. Furthermore, in vitro experiments indicate that SraG inhibits translation initiation of pnp Together, these observations demonstrate that SraG participates in the post-transcriptional control of pnp by a direct antisense interaction between SraG and PNPase RNAs. Our data reveal a new level of regulation in the expression of this major exoribonuclease.
Assuntos
Proteínas de Escherichia coli/genética , Regulação Bacteriana da Expressão Gênica , Polirribonucleotídeo Nucleotidiltransferase/genética , RNA Bacteriano/genética , RNA Interferente Pequeno/genética , Escherichia coli/genética , Escherichia coli/metabolismo , Proteínas de Escherichia coli/metabolismo , Homeostase , Óperon , Polirribonucleotídeo Nucleotidiltransferase/metabolismo , RNA Bacteriano/metabolismo , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , RNA Interferente Pequeno/metabolismoRESUMO
In the fight against pathogenic and opportunistic bacteria, development and spreading of resistance to antibiotics is an increasing public health problem. The available antibacterial treatments are becoming less and less effective, making urgent the discovery of new active molecules. One strategy that has been explored to bypass the bacterial adaptation to drugs is to target the iron metabolism of bacteria, since iron is critical for all bacteria to grow. To date, three major ways have been assessed to exploit weaknesses in the bacterial iron metabolism: the "Trojan Horse strategy" which takes advantages of natural iron-uptake systems to deliver antimicrobial compounds inside the cells; the use of iron-antagonists and iron-chelators in order to reduce iron availability and the inhibition of enzymatic steps of iron metabolism via chemical compounds. This review discusses these antibacterial strategies interfering with several levels of the bacterial iron metabolism, with a special emphasis on recently published and/or patented discoveries.