ライフサイエンスコーパス: SOS response

1 ents results in the induction of the global 'SOS response'.

2 coli, DNA damage elicits the well regulated 'SOS response'.

3 as instigator for this enigmatic HP-induced SOS response.

4 nicity of V. cholerae does not depend on its SOS response.

5 onally toxic substrate vector and induce the SOS response.

6 t that is regulated by LexA cleavage and the SOS response.

7 population of proteins or amounts during the SOS response.

8 nes following stimulation of the V. cholerae SOS response.

9 s activated when PrtR is degraded during the SOS response.

10 , and V) are regulated as part of the global SOS response.

11 , or repair exhibit a partially constitutive SOS response.

12 enes, both of which are involved in the host SOS response.

13 I in the regulation of recombination and the SOS response.

14 maged cells and to constitutively induce the SOS response.

15 ed cell size-both also characteristic of the SOS response.

16 rnal DNA-damaging agents known to induce the SOS response.

17 response, and the cellular repressor of the SOS response.

18 the populations in strains with an inducible SOS response.

19 amage and is dependent on the damage-induced SOS response.

20 d with recombinational DNA repair during the SOS response.

21 aquat, X rays, or conditions that induce the SOS response.

22 esion synthesis as a primary function of the SOS response.

23 lication-blocking DNA lesions as part of the SOS response.

24 A0906, coordinate the Pseudomonas aeruginosa SOS response.

25 uC, MucB, and other proteins involved in the SOS response.

26 ile psiB inhibits induction of the bacterial SOS response.

27 induced following DNA damage as part of the SOS response.

28 on inhibitor SulA (SfiA), a component of the SOS response.

29 lular responses to DNA damage, including the SOS response.

30 of a set of genes known collectively as the SOS response.

31 cation does not result from induction of the SOS response.

32 quinolones, antibiotics that elicit a strong SOS response.

33 -like proteins undergo as part of the global SOS response.

34 uses degradation of DNA and induction of the SOS response.

35 ge tail-like particles upon induction of the SOS response.

36 repair, recombination, and induction of the SOS response.

37 n more complex role of DinI in the bacterial SOS response.

38 te the division blockage associated with the SOS response.

39 r of division that is induced as part of the SOS response.

40 subunits and is up-regulated as part of the SOS response.

41 recA4142 (F217Y) constitutively express the SOS response.

42 a protein-based TA system upregulated by the SOS response.

43 teracts with the LexA repressor inducing the SOS response.

44 t bundles and plays an important role in the SOS response.

45 DNA damage by a mechanism independent of the SOS response.

46 an regulate diverse aspects of the bacterial SOS response.

47 DSBs) than wild type, they do not induce the SOS response.

48 NA repair through induction of the bacterial SOS response.

49 se cells produce DSBs that do not induce the SOS response.

50 ar to be a potent inducer of the V. cholerae SOS response.

51 k, oxidative stress, nitrogen limitation and SOS responses.

52 the known recA-dependent global DNA damage (SOS) response.

53 Upon induction of the SOS response, a 20-fold increase in mutation frequency o

54 w that adaptive mutation is regulated by the SOS response, a complex, graded response to DNA damage t

55 dly evolve resistance to antibiotics via the SOS response, a state of high-activity DNA repair and mu

56 cells lacking aPLs fail to initiate a robust SOS response after DNA damage, indicating that the membr

57 are Rec(+), UV(R) and are able to induce the SOS response after UV treatment like wild-type.

58 nally have a moderate defect in inducing the SOS response after UV treatment.

59 The SOS response aids bacterial propagation by inhibiting ce

60 f colicin E1 is known to be regulated by the SOS response, anaerobiosis, and catabolite repression.

61 with this increase being independent of the SOS response, anaerobiosis, catabolite repression, and i

62 inducible, albeit reduced, activation of the SOS response and a diminished ability to promote cellula

63 ions in priA are chronically induced for the SOS response and are defective in homologous recombinati

64 ion occurs by RepA-mediated induction of the SOS response and can be reversed by over-expression of t

65 ggest that L. pneumophila lacks a prototypic SOS response and competence development in response to g

66 ng PT, including induction of bacteriophage, SOS response and DNA repair-related genes.

67 Similar inductions of the SOS response and PBSX were observed in cells depleted of

68 oved mutant chromosomes due to the mutagenic SOS response and possible recombination of the new allel

69 Major components of repair, SOS response and recombination were identified, includin

70 and R are important for the induction of the SOS response and the formation of RecA*-dependent recomb

71 The RecA-dependent SOS response and the RapI-PhrI cell sensory system activ

72 of Bacillus subtilis and is regulated by the SOS response and the RapI-PhrI cell-cell peptide signali

73 The SOS response and the RapI-PhrI sensory system activate I

74 p between drug-induced oxidative stress, the SOS response and their potential combined contribution t

75 a Mutator Response similar to the bacterial "SOS response" and characterized by the initiation of err

76 causes cell filamentation, induction of the SOS response, and DNA replication arrest in the Gram-neg

77 ation") requires recombination proteins, the SOS response, and error-prone DNA polymerase IV (DinB),

78 h lambda-like phage genes, are induced by an SOS response, and genes involved in the SOS response wer

79 expression of ftsK increased as part of the SOS response, and increased expression of ftsK conferred

80 astic process, which temporarily induces the SOS response, and is followed by DNA repair, maintaining

81 Damage caused by the peptides induces the SOS response, and is synergistic with damage caused by U

82 E. coli, this inducible system is termed the SOS response, and it controls both accurate and potentia

83 pair mutants rule out unbalanced growth, the SOS response, and nucleotide excision repair as explanat

84 ng components of a TTSS are regulated by the SOS response, and our data might explain how a subset of

85 ination, DNA damage repair, induction of the SOS response, and SOS mutagenesis, was found to catalyze

86 air, general recombination, induction of the SOS response, and SOS mutagenesis.

87 ed between FtsZ and SulA, a component of the SOS response, and the interacting regions were mapped to

88 umuDC genes are part of the Escherichia coli SOS response, and their expression is induced as a conse

89 The delta oriL plasmid induces the SOS response, and this is important for plasmid maintena

90 te a predicted role for IsrA and GlmZ in the SOS response, and we expand on current knowledge of the

91 n cancer cells is reminiscent of prokaryotic SOS responses, and further elucidation of these events s

92 /pSK1002 or NM2009 tester strains, using the SOS response as an end point of DNA damage.

93 Pol IV is induced as part of the SOS response, but the effect of GroE on Pol IV was indep

94 ototype antibacterial quinolone, induces the SOS response by a mechanism that requires the RecBCD nuc

95 Induction of the SOS response by the genotoxic antibiotic ciprofloxacin c

96 t pyocin production during the P. aeruginosa SOS response carries both expected and unexpected costs.

97 s Rad6 and Rad18 comparable to the bacterial SOS response, controlling damage-induced transcriptional

98 ction differs from that by which the E. coli SOS response controls induction of many prophages.

99 However, inducing the SOS response does not stimulate transposition.

100 We found that elimination of the SOS response either genetically or by treatment with the

101 erent genetic backgrounds indicated that the SOS response enhances the mutagenicity of M1G and that M

102 ecA protein of Escherichia coli controls the SOS response for DNA damage tolerance and plays a crucia

103 ter gene analyses indicated induction of the SOS response for some of the derivatives, suggesting int

104 Analyses of the SOS response have led to new insights into the transcrip

105 Quinolone treatment induces the bacterial SOS response in a RecBC-dependent manner, arguing that c

106 The SOS response in bacteria includes a global transcription

107 proteins may be part of the LexA-controlled SOS response in bacteria.

108 equences, overproduction of DpiA induced the SOS response in E. coli, suggesting that chromosomal DNA

109 l three base substitution mutations, and the SOS response in Escherichia coli increases bypass of bul

110 The DNA damage-mediated SOS response in Escherichia coli is the best-known examp

111 A by screening for the ability to induce the SOS response in Escherichia coli.

112 recently described negative regulator of the SOS response in Escherichia coli.

113 itution at this position found to induce the SOS response in Escherichia coli.

114 n, indicating that it may be involved in the SOS response in M. tuberculosis.

115 Genotoxic stress induces the RecA-dependent SOS response in many bacteria.

116 The report of an operational SOS response in presumed symbiotic and parasitic bacteri

117 constitutive [recA(Con)] mutants induce the SOS response in the absence of DNA damage.

118 established as the cellular repressor of the SOS response in the bacterium Bacillus subtilis.

119 spectively) and for induction of the E. coli SOS response in the presence of M.HpaII methylation, ind

120 The SOS response in UV-irradiated Escherichia coli includes

121 100 MPa elicits a RecA-dependent DNA damage (SOS) response in Escherichia coli K-12, despite the fact

122 Part of the SOS response includes genes that repair DNA damage, but

123 ull mutation caused partial induction of the SOS response, including induction of the defective proph

124 as an unexpected initiator of the bacterial SOS response, indicate that beta-lactam antibiotics are

125 richia coli is dependent on induction of the SOS response, indicating a role for translesion DNA poly

126 rk damage and exhibit high expression of the SOS response, indicative of repair deficiency.

127 se to cold shock, heat shock, stringent, and SOS response-inducing conditions.

128 ulA, an inhibitor of FtsZ induced during the SOS response, inhibits FtsZ function.

129 ressed state is abolished when the host cell SOS response is activated.

130 The SOS response is an essential process for responding to D

131 ion tolerance events (i) only occur when the SOS response is fully induced and (ii) are executed in c

132 om reporter assays support the idea that the SOS response is influenced by activities associated with

133 ing of the regulation and termination of the SOS response is much more limited.

134 During F plasmid conjugation, however, the SOS response is suppressed by PsiB, an F-plasmid-encoded

135 A hallmark of the Escherichia coli SOS response is the large increase in mutations caused b

136 The induction of the SOS response is well understood and involves the cleavag

137 l V) are expressed late during the bacterial SOS response, it has long been thought that TLS was the

138 ies of recombination crossovers although the SOS-response itself was not induced.

139 The SOS response leads to overexpression of the TisB toxin a

140 Unlike the well-investigated classical SOS response, little is known about newly recognized pat

141 The constitutive induction of the SOS response may be a consequence of the impaired abilit

142 regulation of DinB is the only aspect of the SOS response needed for stress-induced mutagenesis.

143 hat overproduction of Tnp neither induces an SOS response nor a strong heat shock response.

144 enes encoding pyruvate kinase and a putative SOS response nuclease, respectively.

145 Here we discuss the SOS response of E. coli and concentrate in particular on

146 A critical step in the SOS response of Escherichia coli is the specific proteol

147 During the SOS response of Escherichia coli to DNA damage, the umuD

148 hat has been most extensively studied is the SOS response of Escherichia coli.

149 While the SOS response of S. aureus is much more limited than thos

150 We report an analysis of a sample of the SOS response of Salmonella enterica serovar Typhimurium

151 ly on nucA expression by elevating the basal SOS response of the cell.

152 for the observed phenotype: induction of the SOS response or of the heat shock response.

153 d that either the inability to derepress the SOS response or the lack of the LexA-regulated polymeras

154 fluence of negative supercoiling induced the SOS response pathway, and they were recognized as lesion

155 Several commonly used antibiotics induce the SOS response, potentially hastening genetic change and t

156 that described for other inhibitors like the SOS response protein SulA or the moonlighting enzyme Opg

157 Among SOS-response proteins, 25% were ClpXP substrates and, im

158 ed by mutations that prevented the bacterial SOS response (recA mutations) or by enzymes that breakdo

159 We found that the V. cholerae SOS response regulates CTXvphi production.

160 shows amino acid sequence similarity to the SOS response regulator LexA from Escherichia coli.

161 DinI's function in the SOS response remains controversial, since its interactio

162 y, our results indicate that sbcDC, upon the SOS response, represses type 5 capsule production throug

163 tely 4-fold higher than those induced by the SOS response severely impede its growth.

164 1)dG in Escherichia coli is dependent on the SOS response, specifically the umuC and umuD gene produc

165 agent, is a potent inducer of the bacterial SOS response; surprisingly, it has not been used to sele

166 e extensively studied lac operon system, the SOS response system and the araBAD operon system of Esch

167 gene regulation, whereas the results for the SOS response system indicate that the framework is able

168 DNA damage-inducible responses, such as the SOS response, the adaptive response to alkylating agents

169 nal repressor LexA is a key component of the SOS response, the main mechanism for the regulation of D

170 enesis is observed in cells incapable of the SOS response, these data are consistent with the notion

171 t signal transduction system involved in the SOS response to beta-lactams.

172 occurs when pol V is induced as part of the SOS response to DNA damage and incorrectly incorporates

173 tly upregulated as part of the cell's global SOS response to DNA damage and under these conditions, m

174 Bacillus subtilis LexA protein represses the SOS response to DNA damage by binding as a dimer to the

175 The SOS response to DNA damage in bacteria is a well-known c

176 olecules in Escherichia coli and induced the SOS response to DNA damage in E. coli.

177 The SOS response to DNA damage in Escherichia coli involves

178 The V. cholerae SOS response to DNA damage induces the CTX prophage by s

179 The Escherichia coli SOS response to DNA damage is modulated by the RecA prot

180 The SOS response to DNA damage was not induced under these c

181 Activated RecA, the mediator of the host SOS response to DNA damage, causes inactivation of the r

182 on and during the induction of the bacterial SOS response to DNA damage.

183 polB) gene, is induced as part of the global SOS response to DNA damage.

184 protein plays a principal role in bacterial SOS response to DNA damage.

185 gene products is upregulated as part of the SOS response to DNA damage.

186 c translesion DNA synthesis (TLS) during the SOS response to DNA damage.

187 We investigated the SOS response to double-strand breaks in both Escherichia

188 ation complex plays a role in modulating the SOS response to nalidixic acid and that the response is

189 on mutants are specifically deficient in the SOS response to nalidixic acid.

190 in a complementary way to the RecA-dependent SOS response to promote bacterial cell survival to repli

191 RecQ is required for proper induction of the SOS response to replication stress in Escherichia coli.

192 The bacterial SOS response to unusual levels of DNA damage has been re

193 The 'SOS response' to DNA damage alleviates this repression,

194 cell division inhibitor associated with the SOS response, to gain insight into the role of filamento

195 modification, and we confirm binding of the SOS response transcriptional repressor to sites in the p

196 In both cell types, the SOS response was activated, and levels of proteins such

197 Mutants in which the SOS response was constitutively derepressed repaired CPD

198 The SOS response was induced by the addition of mitomycin C

199 Although the SOS response was observed with all three treatments, the

200 ytic pathway, measured in a host lacking the SOS response, was almost undetectably low, probably less

201 ymerase, one that was induced as part of the SOS response, we actually rediscovered DNA polymerase II

202 In addition to the SOS response, we observed the induction of other stress

203 y an SOS response, and genes involved in the SOS response were also regulated by quorum sensing.

204 products, which are up-regulated during the SOS response, were previously shown to bind to the alpha

205 Escherichia coli initiates the SOS response when single-stranded DNA (ssDNA) produced b

206 ollowing DNA damage in bacteria involves the SOS response where cleavage of the transcriptional repre

207 ediated DNA damage activates the V. cholerae SOS response, which in turn likely accounts for ParE's i

208 The potentially deleterious SOS response, which is normally triggered by the appeara

209 ral complex regulatory networks, such as the SOS response, which modifies transcription in response t

210 ther stresses, Escherichia coli utilizes the SOS response, which regulates the expression of at least

211 ion, we found that ciprofloxacin induces the SOS response, which we show, by comparison of a wild-typ

212 he parameters monitored was the induction of SOS responses, which indicate of DNA damage.