scholarly journals Escherichia coli RNA polymerase mutants that enhance or diminish the SOS response constitutively expressed in the absence of RNase HI activity.

1994 ◽  
Vol 176 (5) ◽  
pp. 1521-1523 ◽  
Author(s):  
T Kogoma
Keyword(s):  
Escherichia Coli ◽  
Rna Polymerase ◽  
Sos Response ◽  
Rnase Hi ◽  
Polymerase Mutants

RNA polymerase mutants of Escherichia coli

1976 ◽  
Vol 143 (3) ◽  
pp. 233-241 ◽  
Author(s):  
M. Kawai ◽  
A. Ishihama ◽  
T. Yura
Keyword(s):  
Escherichia Coli ◽  
Rna Polymerase ◽  
Polymerase Mutants

RNA polymerase mutants of Escherichia coli

1973 ◽  
Vol 121 (2) ◽  
pp. 181-196 ◽  
Author(s):  
Y. Iwakura ◽  
A. Ishihama ◽  
T. Yura
Keyword(s):  
Escherichia Coli ◽  
Rna Polymerase ◽  
Polymerase Mutants

scholarly journals RNA polymerase mutants found through adaptive evolution reprogram Escherichia coli for optimal growth in minimal media

2010 ◽  
Vol 107 (47) ◽  
pp. 20500-20505 ◽  
Author(s):  
T. M. Conrad ◽  
M. Frazier ◽  
A. R. Joyce ◽  
B.-K. Cho ◽  
E. M. Knight ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Rna Polymerase ◽  
Adaptive Evolution ◽  
Optimal Growth ◽  
Minimal Media ◽  
Polymerase Mutants

scholarly journals Identification of genes involved in low aminoglycoside-induced SOS response in Vibrio cholerae: a role for transcription stalling and Mfd helicase

2013 ◽  
Vol 42 (4) ◽  
pp. 2366-2379 ◽  
Author(s):  
Zeynep Baharoglu ◽  
Anamaria Babosan ◽  
Didier Mazel
Keyword(s):  
Escherichia Coli ◽  
Rna Polymerase ◽  
Vibrio Cholerae ◽  
Sos Response ◽  
Genetic Screen ◽  
Dna Lesions ◽  
Gene Overexpression ◽  
Sos Induction ◽  
Complex Reconstruction ◽  
Oxidized Guanine

Abstract Sub-inhibitory concentrations (sub-MIC) of antibiotics play a very important role in selection and development of resistances. Unlike Escherichia coli, Vibrio cholerae induces its SOS response in presence of sub-MIC aminoglycosides. A role for oxidized guanine residues was observed, but the mechanisms of this induction remained unclear. To select for V. cholerae mutants that do not induce low aminoglycoside-mediated SOS induction, we developed a genetic screen that renders induction of SOS lethal. We identified genes involved in this pathway using two strategies, inactivation by transposition and gene overexpression. Interestingly, we obtained mutants inactivated for the expression of proteins known to destabilize the RNA polymerase complex. Reconstruction of the corresponding mutants confirmed their specific involvement in induction of SOS by low aminoglycoside concentrations. We propose that DNA lesions formed on aminoglycoside treatment are repaired through the formation of single-stranded DNA intermediates, inducing SOS. Inactivation of functions that dislodge RNA polymerase leads to prolonged stalling on these lesions, which hampers SOS induction and repair and reduces viability under antibiotic stress. The importance of these mechanisms is illustrated by a reduction of aminoglycoside sub-MIC. Our results point to a central role for transcription blocking at DNA lesions in SOS induction, so far underestimated.

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