Journal of Bacteriology, August 2001, p. 4543-4550, Vol. 183, No. 15
0021-9193/01/$04.00+0 DOI: 10.1128/JB.183.15.4543-4550.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Departamento de Bioquímica de la Nutrición, Instituto Superior de Investigaciones Biológicas (Consejo Nacional de Investigaciones Cientificas y Técnicas-Universidad Nacional de Tucumán), and Instituto de Química Biológica "Dr. Bernabé Bloj," Chacabuco 461, 4000 San Miguel de Tucumán, Tucumán, Argentina
Received 30 April 2001/Accepted 10 May 2001
Escherichia coli microcin J25 (MccJ25) is a
plasmid-encoded, cyclic peptide antibiotic consisting of 21 unmodified
amino acid residues. It is primarily active on gram-negative bacteria
related to the producer strain, inducing cell filamentation in an
SOS-independent way. A mutation causing resistance to MccJ25 was
isolated. Genetic analysis indicated that it resided in the
rpoC gene, encoding the
' subunit of RNA polymerase, at
90 min on the E. coli genetic map. The mutation was
genetically crossed on to a plasmid containing the wild-type
rpoC gene. The presence of the recombinant plasmid conferred complete resistance to otherwise sensitive strains. Nucleotide sequencing of the plasmid-borne, mutant rpoC
gene revealed a ACC (Thr)-to-ATC (Ile) change at codon 931, within
homology block G, an evolutionarily conserved region in the large
subunits of all RNA polymerases. MccJ25 decreased RNA synthesis both in vivo and in vitro. These results point to the RNA polymerase as the
target of microcin action. We favor the possibility that the filamentous phenotype induced by MccJ25 results from impaired transcription of genes coding for cell division proteins. As far as we
know, MccJ25 is the first peptide antibiotic shown to affect RNA polymerase.
This article has been cited by other articles:
| Appl. Environ. Microbiol. | Infect. Immun. | Eukaryot. Cell |
|---|---|---|
| Mol. Cell. Biol. | J. Virol. | Microbiol. Mol. Biol. Rev. |
| ALL ASM JOURNALS |