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1 ents results in the induction of the global 'SOS response'.
2 coli, DNA damage elicits the well regulated 'SOS response'.
3 the DNA-damage response in Escherichia coli (SOS response).
4 an regulate diverse aspects of the bacterial SOS response.
5 DSBs) than wild type, they do not induce the SOS response.
6 NA repair through induction of the bacterial SOS response.
7 se cells produce DSBs that do not induce the SOS response.
8 ar to be a potent inducer of the V. cholerae SOS response.
9 nicity of V. cholerae does not depend on its SOS response.
10 onally toxic substrate vector and induce the SOS response.
11 t that is regulated by LexA cleavage and the SOS response.
12 population of proteins or amounts during the SOS response.
13 nes following stimulation of the V. cholerae SOS response.
14 s activated when PrtR is degraded during the SOS response.
15 , and V) are regulated as part of the global SOS response.
16 , or repair exhibit a partially constitutive SOS response.
17 enes, both of which are involved in the host SOS response.
18 I in the regulation of recombination and the SOS response.
19 mage via its multiple roles in the bacterial SOS response.
20 maged cells and to constitutively induce the SOS response.
21 ed cell size-both also characteristic of the SOS response.
22 rnal DNA-damaging agents known to induce the SOS response.
23 response, and the cellular repressor of the SOS response.
24 the populations in strains with an inducible SOS response.
25 amage and is dependent on the damage-induced SOS response.
26 d with recombinational DNA repair during the SOS response.
27 aquat, X rays, or conditions that induce the SOS response.
28 lication-blocking DNA lesions as part of the SOS response.
29 uC, MucB, and other proteins involved in the SOS response.
30 ile psiB inhibits induction of the bacterial SOS response.
31 induced following DNA damage as part of the SOS response.
32 on inhibitor SulA (SfiA), a component of the SOS response.
33 lular responses to DNA damage, including the SOS response.
34 of a set of genes known collectively as the SOS response.
35 cation does not result from induction of the SOS response.
36 ormation of a RecA-ssDNA filament during the SOS response.
37 -like proteins undergo as part of the global SOS response.
38 uses degradation of DNA and induction of the SOS response.
39 xA-controlled division inhibition during the SOS response.
40 uces lytic development through the bacterial SOS response.
41 sed fluoroquinolones are known to induce the SOS response.
42 ally delayed with respect to the peak of the SOS response.
43 directly or indirectly, which activates the SOS response.
44 increased membrane permeability and provoked SOS response.
45 estart, or activation of the transcriptional SOS response.
46 as instigator for this enigmatic HP-induced SOS response.
47 t bundles and plays an important role in the SOS response.
48 esion synthesis as a primary function of the SOS response.
49 A0906, coordinate the Pseudomonas aeruginosa SOS response.
50 quinolones, antibiotics that elicit a strong SOS response.
51 ge tail-like particles upon induction of the SOS response.
52 repair, recombination, and induction of the SOS response.
53 n more complex role of DinI in the bacterial SOS response.
54 te the division blockage associated with the SOS response.
55 r of division that is induced as part of the SOS response.
56 subunits and is up-regulated as part of the SOS response.
57 recA4142 (F217Y) constitutively express the SOS response.
58 a protein-based TA system upregulated by the SOS response.
59 teracts with the LexA repressor inducing the SOS response.
60 DNA damage by a mechanism independent of the SOS response.
61 k, oxidative stress, nitrogen limitation and SOS responses.
62 the known recA-dependent global DNA damage (SOS) response.
65 w that adaptive mutation is regulated by the SOS response, a complex, graded response to DNA damage t
66 dly evolve resistance to antibiotics via the SOS response, a state of high-activity DNA repair and mu
67 amage DNA in persisters and that the ensuing SOS response accelerates the development of antibiotic r
69 cells lacking aPLs fail to initiate a robust SOS response after DNA damage, indicating that the membr
73 f colicin E1 is known to be regulated by the SOS response, anaerobiosis, and catabolite repression.
74 with this increase being independent of the SOS response, anaerobiosis, catabolite repression, and i
75 inducible, albeit reduced, activation of the SOS response and a diminished ability to promote cellula
77 ions in priA are chronically induced for the SOS response and are defective in homologous recombinati
78 ion occurs by RepA-mediated induction of the SOS response and can be reversed by over-expression of t
79 ggest that L. pneumophila lacks a prototypic SOS response and competence development in response to g
81 playing distinct gene expression patterns of SOS response and metabolic pathways in E. coli populatio
83 oved mutant chromosomes due to the mutagenic SOS response and possible recombination of the new allel
84 em with a novel inhibitor could suppress the SOS response and potentially reduce the occurrence of AM
86 iveness of different antibiotics in blocking SOS response and Stx1/2 production, we constructed a rep
87 and R are important for the induction of the SOS response and the formation of RecA*-dependent recomb
89 of Bacillus subtilis and is regulated by the SOS response and the RapI-PhrI cell-cell peptide signali
91 p between drug-induced oxidative stress, the SOS response and their potential combined contribution t
92 a Mutator Response similar to the bacterial "SOS response" and characterized by the initiation of err
93 causes cell filamentation, induction of the SOS response, and DNA replication arrest in the Gram-neg
94 ation") requires recombination proteins, the SOS response, and error-prone DNA polymerase IV (DinB),
95 ualinium, which also indirectly inhibits the SOS response, and found it had a strong ability to inhib
96 h lambda-like phage genes, are induced by an SOS response, and genes involved in the SOS response wer
97 expression of ftsK increased as part of the SOS response, and increased expression of ftsK conferred
98 astic process, which temporarily induces the SOS response, and is followed by DNA repair, maintaining
99 Damage caused by the peptides induces the SOS response, and is synergistic with damage caused by U
100 E. coli, this inducible system is termed the SOS response, and it controls both accurate and potentia
101 pair mutants rule out unbalanced growth, the SOS response, and nucleotide excision repair as explanat
102 ng components of a TTSS are regulated by the SOS response, and our data might explain how a subset of
103 ination, DNA damage repair, induction of the SOS response, and SOS mutagenesis, was found to catalyze
105 ed between FtsZ and SulA, a component of the SOS response, and the interacting regions were mapped to
106 umuDC genes are part of the Escherichia coli SOS response, and their expression is induced as a conse
108 te a predicted role for IsrA and GlmZ in the SOS response, and we expand on current knowledge of the
109 n cancer cells is reminiscent of prokaryotic SOS responses, and further elucidation of these events s
110 ndancy within the circuit, modulation of the SOS response, antibiotic-independent plasmid maintenance
111 physiological environment and highlights the SOS response as a possible mechanism that contributes to
113 utionary conservation of its catalytic SRAP (SOS Response Associated Peptidase) domain, the enzymatic
115 report crystal structures of the human HMCES SOS response-associated peptidase (SRAP) domain in compl
117 s filament extensively and induce impressive SOS responses before returning to a normal appearance.
118 ncentrations of ciprofloxacin did induce the SOS response, but not when the cells were exposed to rif
120 ototype antibacterial quinolone, induces the SOS response by a mechanism that requires the RecBCD nuc
122 t pyocin production during the P. aeruginosa SOS response carries both expected and unexpected costs.
123 s Rad6 and Rad18 comparable to the bacterial SOS response, controlling damage-induced transcriptional
125 major classes of antibiotics may induce the SOS response could have worthwhile implications for anti
129 erent genetic backgrounds indicated that the SOS response enhances the mutagenicity of M1G and that M
130 erstanding of the importance of a functional SOS response for bacterial fitness in the context of a c
131 ecA protein of Escherichia coli controls the SOS response for DNA damage tolerance and plays a crucia
132 ter gene analyses indicated induction of the SOS response for some of the derivatives, suggesting int
133 This response operates independently of the SOS response, governs the expression of genes crucial fo
138 a new class of repressors orchestrating the SOS response illuminates long-standing questions regardi
139 Quinolone treatment induces the bacterial SOS response in a RecBC-dependent manner, arguing that c
142 equences, overproduction of DpiA induced the SOS response in E. coli, suggesting that chromosomal DNA
143 -binding proteins following induction of the SOS response in Enterobacter cloacae decreased the amoun
144 l three base substitution mutations, and the SOS response in Escherichia coli increases bypass of bul
151 terial pathogenesis, and yet the role of the SOS response in nonpathogenic organisms and in physiolog
156 spectively) and for induction of the E. coli SOS response in the presence of M.HpaII methylation, ind
157 he aminoglycosides become able to induce the SOS response in this species, thus leading to the elevat
160 100 MPa elicits a RecA-dependent DNA damage (SOS) response in Escherichia coli K-12, despite the fact
163 ull mutation caused partial induction of the SOS response, including induction of the defective proph
164 In Escherichia coli, after DNA damage, the SOS response increases the transcription (and protein le
165 as an unexpected initiator of the bacterial SOS response, indicate that beta-lactam antibiotics are
166 richia coli is dependent on induction of the SOS response, indicating a role for translesion DNA poly
174 Our findings show that the induction of the SOS response is due to nitric oxide (NO) accumulation in
175 ion tolerance events (i) only occur when the SOS response is fully induced and (ii) are executed in c
177 om reporter assays support the idea that the SOS response is influenced by activities associated with
179 During F plasmid conjugation, however, the SOS response is suppressed by PsiB, an F-plasmid-encoded
183 l V) are expressed late during the bacterial SOS response, it has long been thought that TLS was the
188 ution of CTX prophage in the essentiality of SOS response master regulator LexA, which is otherwise n
190 regulation of DinB is the only aspect of the SOS response needed for stress-induced mutagenesis.
198 We report an analysis of a sample of the SOS response of Salmonella enterica serovar Typhimurium
201 d that either the inability to derepress the SOS response or the lack of the LexA-regulated polymeras
202 sphate/tetraphosphate (henceforth ppGpp) and SOS response pathway involved in the formation of persis
203 fluence of negative supercoiling induced the SOS response pathway, and they were recognized as lesion
204 erichia coli strain, MP1, we showed that the SOS response plays a vital role during colonization of t
205 Several commonly used antibiotics induce the SOS response, potentially hastening genetic change and t
206 that described for other inhibitors like the SOS response protein SulA or the moonlighting enzyme Opg
208 ed by mutations that prevented the bacterial SOS response (recA mutations) or by enzymes that breakdo
209 time-resolved, simultaneous read-out of the SOS response (recAP-cfp) and Stx1 production (stx1::yfp)
210 that when produced at high levels during the SOS response, RecN interferes with nucleoid partitioning
216 y, our results indicate that sbcDC, upon the SOS response, represses type 5 capsule production throug
218 1)dG in Escherichia coli is dependent on the SOS response, specifically the umuC and umuD gene produc
219 -23) and that cell subpopulations induce the SOS response spontaneously even in the absence of stress
221 agent, is a potent inducer of the bacterial SOS response; surprisingly, it has not been used to sele
222 e extensively studied lac operon system, the SOS response system and the araBAD operon system of Esch
223 gene regulation, whereas the results for the SOS response system indicate that the framework is able
225 existence of a noncanonical mechanism beyond SOS-response that is controlled by the intracellular oxi
226 DNA damage-inducible responses, such as the SOS response, the adaptive response to alkylating agents
228 r stress conditions such as induction of the SOS response, the association of DNA polymerase IV with
229 nal repressor LexA is a key component of the SOS response, the main mechanism for the regulation of D
230 equently hindering its cleavage, suppressing SOS response thereby reducing mutation frequency and AMR
231 enesis is observed in cells incapable of the SOS response, these data are consistent with the notion
232 cteria, this coordination is mediated by the SOS response through LexA, which triggers a halt in cell
234 These mutations require the induction of the SOS response to DNA damage and display a distinct patter
235 occurs when pol V is induced as part of the SOS response to DNA damage and incorrectly incorporates
236 tly upregulated as part of the cell's global SOS response to DNA damage and under these conditions, m
237 Bacillus subtilis LexA protein represses the SOS response to DNA damage by binding as a dimer to the
244 mbda CI repressor, is inactivated during the SOS response to DNA damage, and this regulation ensures
245 Activated RecA, the mediator of the host SOS response to DNA damage, causes inactivation of the r
252 ation complex plays a role in modulating the SOS response to nalidixic acid and that the response is
254 in a complementary way to the RecA-dependent SOS response to promote bacterial cell survival to repli
255 RecQ is required for proper induction of the SOS response to replication stress in Escherichia coli.
258 cell division inhibitor associated with the SOS response, to gain insight into the role of filamento
259 modification, and we confirm binding of the SOS response transcriptional repressor to sites in the p
264 ytic pathway, measured in a host lacking the SOS response, was almost undetectably low, probably less
265 ymerase, one that was induced as part of the SOS response, we actually rediscovered DNA polymerase II
267 hia coli, which later came to be called the "SOS response." We revisited this response using the repl
268 y an SOS response, and genes involved in the SOS response were also regulated by quorum sensing.
269 products, which are up-regulated during the SOS response, were previously shown to bind to the alpha
271 ollowing DNA damage in bacteria involves the SOS response where cleavage of the transcriptional repre
272 entially targeted, due to its involvement in SOS response which is majorly responsible for adaptive m
273 ediated DNA damage activates the V. cholerae SOS response, which in turn likely accounts for ParE's i
275 ral complex regulatory networks, such as the SOS response, which modifies transcription in response t
276 ther stresses, Escherichia coli utilizes the SOS response, which regulates the expression of at least
277 ion, we found that ciprofloxacin induces the SOS response, which we show, by comparison of a wild-typ