ライフサイエンスコーパス: smegmatis

1 termined against Mycobacterium smegmatis (M. smegmatis).

2 m in both Escherichia coli and Mycobacterium smegmatis.

3 eprae SodC (rSodC) produced in Mycobacterium smegmatis.

4 ing in vitro and inhibit FtsX function in M. smegmatis.

5 -glutamate for peptidoglycan synthesis in M. smegmatis.

6 erium tuberculosis, but not in Mycobacterium smegmatis.

7 in the fast-growing surrogate, Mycobacterium smegmatis.

8 d the inner membrane lipids of Mycobacterium smegmatis.

9 at determines conjugal mating identity in M. smegmatis.

10 rculosis, Escherichia coli and Mycobacterium smegmatis.

11 of cytokines in macrophages infected with M. smegmatis.

12 sis and its avirulent relative Mycobacterium smegmatis.

13 utant was distinct from that by wild-type M. smegmatis.

14 of lipids in the microorganism Mycobacterium smegmatis.

15 /Mn-superoxide dismutase, particularly in M. smegmatis.

16 ress beta-lactam resistance in Mycobacterium smegmatis.

17 proteins of the model organism Mycobacterium smegmatis.

18 Mycobacterium tuberculosis and Mycobacterium smegmatis.

19 al role of the CtpD protein of Mycobacterium smegmatis.

20 stablishment of the MtbESX-1 apparatus in M. smegmatis.

21 sis and its avirulent relative Mycobacterium smegmatis.

22 nced yellow fluorescent protein (EYFP) in M. smegmatis.

23 gene cluster ortholog found in Mycobacterium smegmatis.

24 cell, and cell pole regions in Mycobacterium smegmatis.

25 tion of antioxidant defense mechanisms in M. smegmatis.

26 ately 93% is sufficient to cause death of M. smegmatis.

27 ophores under low-iron conditions than wt M. smegmatis.

28 also identified in M. tuberculosis and/or M. smegmatis.

29 nt was reduced compared to wild-type (wt) M. smegmatis.

30 nt for proper cell division in Mycobacterium smegmatis.

31 d impact on growth of M. tuberculosis and M. smegmatis.

32 ransfer process that occurs in Mycobacterium smegmatis.

33 se uptake and growth of a porin mutant of M. smegmatis.

34 second (p)ppGpp synthetase in Mycobacterium smegmatis.

35 y (OD) from micro cultures of E. coli and M. smegmatis.

36 gence of the hemerythrin-like proteins in M. smegmatis.

37 including the closely related Mycobacterium smegmatis.

38 ed, and compared 627 phages of Mycobacterium smegmatis.

39 ts ortholog from nonpathogenic Mycobacterium smegmatis.

40 xpressed in the surrogate host Mycobacterium smegmatis.

41 terized the MceG orthologue of Mycobacterium smegmatis.

42 lude the fast-growing organism Mycobacterium smegmatis.

43 ortant peroxide stress response system in M. smegmatis.

44 of one or more of the 28 sigma factors in M. smegmatis.

45 air elevated the invasion and survival of M. smegmatis 2-3-fold in secondary cell lines in the presen

46 cum (5.20 +/- 0.20 kV/cm), and Mycobacterium smegmatis (5.56 +/- 0.08 kV/cm) have been successfully c

47 Expression of the lprI gene in Mycobacterium smegmatis (8-10-fold) protected its growth from lysozyme

48 creating a DeltamurI strain of Mycobacterium smegmatis, a close relative of Mycobacterium tuberculosi

49 protein pupylation by PafA in Mycobacterium smegmatis, a model mycobacterial organism.

50 vation that a mutant strain of Mycobacterium smegmatis, a nonpathogenic relative of M. tuberculosis,

51 aerobe, the soil actinomycete Mycobacterium smegmatis, adopts an anaerobe-type strategy by activatin

52 responsible for the natural resistance of M. smegmatis against 3.

53 to determine the resistance mechanism of M. smegmatis against one hit, 3-bromo-N-(5-nitrothiazol-2-y

54 iii) RnhB and RnhA collaborate to protect M. smegmatis against oxidative damage in stationary phase.

55 TA domain is dispensable in the avirulent M. smegmatis, all four PASTA domains are essential in M. tu

56 trast, LPS, monosodium urate crystals, or M. smegmatis alone had no activity.

57 hat the Cpn60.2 homologue from Mycobacterium smegmatis also fails to oligomerize under standard condi

58 verexpression of the proteins is toxic to M. smegmatis, although whether this toxicity and the associ

59 ression of Rv3802 orthologs in Mycobacterium smegmatis and Corynebacterium glutamicum increases mycol

60 C16:0 (sn-2) GlcAGroAc2 glycolipids from M. smegmatis and Corynebacterium glutamicum.

61 fferences of esx-3 in M. tuberculosis and M. smegmatis and demonstrate the importance of metal-depend

62 n the nonpathogenic saprophyte Mycobacterium smegmatis and in the human pathogen Mtb by inactivating

63 Deletion of pepD or mprAB in Mycobacterium smegmatis and M. tuberculosis alters the stress response

64 b2 treatment impairs membrane function of M. smegmatis and M. tuberculosis cells.

65 Here we show that Mycobacterium smegmatis and M. tuberculosis strains lacking Rv1422 hav

66 Gfp expression and fluorescence of M. smegmatis and M. tuberculosis strains with multiple inte

67 ite the near sequence identity of MtrA in M. smegmatis and M. tuberculosis, the M. smegmatis oriC is

68 ated recombinant genes in both Mycobacterium smegmatis and M. tuberculosis, with maximal promoter act

69 sisters, within populations of Mycobacterium smegmatis and M. tuberculosis.

70 vity to 2-deoxy-galactose (2-DOG) in both M. smegmatis and M. tuberculosis.

71 he time to generate unmarked mutations in M. smegmatis and M. tuberculosis.

72 MspA is the major porin of Mycobacterium smegmatis and mediates diffusion of small and hydrophili

73 macrophages infected with esxL-expressing M. smegmatis and mouse splenocytes led to down-regulation o

74 Analysis of Mycobacterium smegmatis and Mycobacterium bovis bacille Calmette-Gueri

75 of reporter gene activities in Mycobacterium smegmatis and Mycobacterium bovis BCG.

76 Mycobacterium smegmatis and Mycobacterium kansasii were used as models

77 tB sites in the chromosomes of Mycobacterium smegmatis and Mycobacterium tuberculosis yielded identic

78 unterselectable marker in both Mycobacterium smegmatis and Mycobacterium tuberculosis.

79 eport here that the genomes of Mycobacterium smegmatis and other soil mycobacteria contain an additio

80 d in the environmental niches occupied by M. smegmatis and other soil-dwelling mycobacteria.

81 ed all three hemerythrin-like proteins in M. smegmatis and our results identified and characterized t

82 er assays using membranes from Mycobacterium smegmatis and purified PimA and PimB' indicated that the

83 intracellular and extracellular growth of M. smegmatis and slow-growing M. bovis BCG.

84 The GlgE orthologues from Mycobacterium smegmatis and Streptomyces coelicolor were phosphorylate

85 Here, we purified LM from the avirulent M. smegmatis and the virulent M. tuberculosis H(37)R(v), pe

86 e to mediate LAM production in Mycobacterium smegmatis and were unable to complement an embC deletion

87 le-cell level in Mycobacterium smegmatis (M. smegmatis) and Mycobacterium bovis Bacillus Calmette-Gue

88 codon usage (Escherichia coli, Mycobacterium smegmatis, and Bacillus subtilis), we show that the freq

89 DnaK is essential in Mycobacterium smegmatis, and ClpB is involved in asymmetrically distri

90 A toxins, in Escherichia coli, Mycobacterium smegmatis, and M. tuberculosis.

91 ilis, Streptomyces coelicolor, Mycobacterium smegmatis, and Pseudomonas aeruginosa.

92 for Co(2)(+) and Ni(2)(+) homeostasis in M. smegmatis, and that M. tuberculosis CtpD orthologue coul

93 2) in the natural product from Mycobacterium smegmatis, and the structural assignment of related C18:

94 ts antibiotic activity against Mycobacterium smegmatis, and this loss in bioactivity is primarily due

95 GPLs from Mycobacterium smegmatis are composed of a lipopeptide core unit consis

96 Here, we show that the Msp porins of M. smegmatis are involved in the acquisition of soluble iro

97 -based extrachromosomal plasmids is 23 in M. smegmatis as determined by quantitative real-time PCR an

98 C caused similar phenotypes in Mycobacterium smegmatis, as expected for genes in a single pathway.

99 first apo-MbtA structure from Mycobacterium smegmatis at 2.3 A.

100 from both M. tuberculosis and Mycobacterium smegmatis at a homologous cut site in vitro.

101 growing mycobacterial species Mycobacterium smegmatis bearing an intact esx-3 locus were rapidly let

102 Here we show that the FM in Mycobacterium smegmatis biofilms is produced through the enzymatic rel

103 Growth of Mycobacterium smegmatis biofilms requires multiple factors including a

104 s are expressed upon RedRock infection of M. smegmatis, but are downregulated once lysogeny is establ

105 genetically modified strain of Mycobacterium smegmatis called IKEPLUS is a promising TB vaccine candi

106 n become available, suggesting Mycobacterium smegmatis can switch between fermentation, anaerobic res

107 lation-defective PknK(Mtb), in Mycobacterium smegmatis cause significant retardation of the growth ra

108 cleavage activities were identified from M. smegmatis cell extracts.

109 omains and the full-length Lysin A caused M. smegmatis cell lysis.

110 The LAM content of the M. smegmatis cell wall was dramatically reduced as the baci

111 impaired IL-8 expression upon exposure to M. smegmatis Collectively, our results indicate that the R7

112 verexpression of recombinant TopoI-CTD in M. smegmatis competed with the endogenous topoisomerase I f

113 versely, expression of ppgS in Mycobacterium smegmatis conferred upon this species otherwise devoid o

114 report that cydAB and cydDC in Mycobacterium smegmatis constitute two separate operons under hypoxic

115 All together, our results show that M. smegmatis constitutively encodes an Na(+)-dependent MATE

116 Mycobacterium smegmatis contains 6 homologous mce (mammalian cell entr

117 er membrane of the saprophytic Mycobacterium smegmatis contains the Msp family of porins, which enabl

118 Mycobacterium smegmatis contains three hemerythrin-like proteins, MSME

119 Mycobacterium smegmatis contains three putative TA systems, VapBC, Maz

120 The deletion of the murI gene in M. smegmatis could be achieved only in minimal medium suppl

121 are also expressed in the non-pathogenic M. smegmatis could be functioning to regulate conserved cel

122 proteins, can complement for loss of the M. smegmatis cpn60.1 gene.

123 Deletion of M. tuberculosis or Mycobacterium smegmatis ctpC leads to cytosolic Mn(2+) accumulation bu

124 Co(2+) and Fe(2+) Mutation of Mycobacterium smegmatis ctpJ affects the homeostasis of both ions.

125 radical scavenger thiourea, when added to M. smegmatis cultures maintained at high DO levels, rescues

126 has been detected in M. tuberculosis and M. smegmatis cultures.

127 also showed that the presence of P27 from M. smegmatis decreases the association of LAMP-3 with bead

128 We show here that an M. smegmatis Delta ponA2 mutant has an unusual antibiotic s

129 A M. smegmatis DeltacrgA strain exhibited a bulged cell morph

130 us were rapidly lethal, infection with an M. smegmatis Deltaesx-3 mutant (here designated as the IKE

131 This study unveils Mycobacterium smegmatis DinB2 as the founder of a clade of Y-family DN

132 Mycobacterium smegmatis DinB2 is the founder of a clade of Y-family DN

133 The mshA::Tn5 mutant of Mycobacterium smegmatis does not produce mycothiol (MSH) and was found

134 t the pore interface unique to Mycobacterium smegmatis Dps protein, MsDps2.

135 e successfully overexpressed and purified M. smegmatis EgtE enzyme and evaluated its activities under

136 ted with the overexpression of Mycobacterium smegmatis EgtE protein, the proposed EgtE functionality

137 Mycobacterium smegmatis encodes four RNase H enzymes: RnhA, RnhB, RnhC

138 Mycobacterium tuberculosis and Mycobacterium smegmatis, encompass substantial genetic diversity and a

139 nt of Escherichia coli and its Mycobacterium smegmatis equivalent (GyrA-G89C).

140 mannosyltransferase PimA, from Mycobacteria smegmatis , establishes the requirement of the EX(7)E mo

141 tuberculosis (EsxG and EsxH), Mycobacterium smegmatis (EsxA and EsxB), and Corynebacterium diphtheri

142 The model mycobacterium Mycobacterium smegmatis executes homologous recombination in the absen

143 Our data suggest that M. smegmatis expresses two PNPs: a previously described tri

144 ribosyltransferase activity in Mycobacterium smegmatis expressing recombinant Rv3242c (MsmRv3242c) co

145 The elevated expression of HbN in Mtb and M. smegmatis facilitated their entry within the macrophages

146 e executed a genetic screen in Mycobacterium smegmatis for biotin auxotrophs and identified pyruvate

147 rcalating in DNA and impaired recovery of M. smegmatis from UV irradiation.

148 en for their ability to delay recovery of M. smegmatis from UV irradiation.

149 uorescens, gi 70731221 ; anti, Mycobacterium smegmatis, gi 118470554 ) document that the conserved Ly

150 Complementation studies of a M. smegmatis glgE mutant strain with these GlgE derivatives

151 tes in the phnD-phnF intergenic region of M. smegmatis has allowed us to propose a quantitative model

152 We show that Mycobacterium smegmatis has an enzyme catalyzing transfer of maltose f

153 Here we demonstrate that Mycobacterium smegmatis has three DSB repair pathway options: HR, NHEJ

154 Surprisingly, M. smegmatis has three paralogs of SMC proteins: EptC and M

155 , including M. bovis BCG, M. marinum, and M. smegmatis have significantly contributed to understandin

156 cture of MsAcg (MSMEG_5246), a Mycobacterium smegmatis homologue of Mycobacterium tuberculosis Acg (R

157 ssion in the heterologous host Mycobacterium smegmatis in a way that requires metal site 1.

158 nd the beta' subunit of RNA polymerase of M. smegmatis in the absence of DNA.

159 rystal structures of PatA from Mycobacterium smegmatis in the presence of its naturally occurring acy

160 dRock forms stable lysogens in Mycobacterium smegmatis in which the prophage replicates at 2.4 copies

161 t provide redundant capabilities and that M. smegmatis, in contrast with Mycobacterium tuberculosis,

162 hal to Helicobacter pylori and Mycobacterium smegmatis, indicating that DapE's are essential for cell

163 nvirulent mycobacteria such as Mycobacterium smegmatis induce AIM2 inflammasome activation, which is

164 In contrast, SmegLM and live M. smegmatis induce high miR-155 expression and low miR-125

165 that the cellular concentration of LAM in M. smegmatis is selectively modulated with the growth phase

166 orter encoded by the genome of Mycobacterium smegmatis is stabilized by d-threitol.

167 smembrane channel protein from Mycobacterium smegmatis, is one of the most stable proteins known to d

168 e lysine acyltransferases from Mycobacterium smegmatis (KATms) and Mycobacterium tuberculosis (KATmt)

169 10 uM) are required to observe Mycobacterium smegmatis killing.

170 this system, we constructed a conditional M. smegmatis knockdown mutant in which addition of anhydrot

171 We showed previously that M. smegmatis lacking MmpL11 has reduced membrane permeabili

172 Here, we identify and characterize M. smegmatis Lhr as the exemplar of a novel clade of superf

173 st bacilli, while in the stationary phase M. smegmatis lost the characteristic rod shape and develope

174 mics at a single-cell level in Mycobacterium smegmatis (M. smegmatis) and Mycobacterium bovis Bacillu

175 vities were determined against Mycobacterium smegmatis (M. smegmatis).

176 cobacterium smegmatis Upon infection with M. smegmatis, macrophages from knock-in mice harboring R753

177 The high G6P level in Mycobacterium smegmatis may result from 10-25-fold higher activity of

178 When expressed in noninvasive Mycobacterium smegmatis, MBP-1 increased the ability of the bacteria t

179 acterium bovis BCG Pasteur and Mycobacterium smegmatis mc(2) 155.

180 d 49% of ORFs of M. bovis BCG Pasteur and M. smegmatis mc(2) 155.

181 o infect a single common host, Mycobacterium smegmatis mc(2) 155.

182 als, we studied this gene (MSMEG_2631) in M. smegmatis mc(2)155 and determined that it encodes a MATE

183 ts, that the soil actinomycete Mycobacterium smegmatis mc(2)155 constitutively oxidizes subtropospher

184 ered that the inducer molecule of KstR in M. smegmatis mc(2)155 is not cholesterol but 3-oxo-4-choles

185 ages infecting the common host Mycobacterium smegmatis mc(2)155 shows that they span considerable gen

186 ages that can infect the host, Mycobacterium smegmatis mc(2)155.

187 The growth of the porin triple mutant M. smegmatis ML16 in media with limiting amounts of nitrate

188 erein the further characterization of the M. smegmatis mmpL11 mutant and identification of the MmpL11

189 Phenotypes of the M. smegmatis mmpL11 mutant are complemented by the expressi

190 We found that biofilm formation by the M. smegmatis mmpL11 mutant was distinct from that by wild-t

191 report the characterization of Mycobacterium smegmatis MmpL11.

192 lly related ESX-1 apparatus of Mycobacterium smegmatis (Ms) to show that fluorescently tagged protein

193 ous ESAT-6 from non-pathogenic Mycobacterium smegmatis (MsESAT-6) was essentially inactive in release

194 Recombinant Mycobacterium smegmatis MshC catalyzes the ATP-dependent condensation

195 otein improves the survival of Mycobacterium smegmatis (Msm) in macrophages and functions as the acet

196 olution crystal structure of a Mycobacterium smegmatis (Msm) open promoter complex (RPo), along with

197 tide quinones (PkQs) from both Mycobacterium smegmatis (Msmeg) and Mtb.

198 The M. smegmatis MSMEG_0023 crgA double mutant strain showed se

199 Deletion of the Rv0008c homolog in M. smegmatis, MSMEG_0023, caused bulged cell poles, formati

200 t exposure to an esterase from Mycobacterium smegmatis (Msmeg_1529), hydrolyzing the ester linkage of

201 pressed in Escherichia coli or Mycobacterium smegmatis, MtbFHb remained associated with the cell memb

202 The M. smegmatis mtrB mutant was filamentous, defective for cel

203 is sensitive to extracellular Zn(2+), the M. smegmatis mutant is not.

204 Similar phenotypes were observed for a M. smegmatis mutant lacking the homolog Ms3747, demonstrati

205 An M. smegmatis mutant strain lacking the ctpD gene was hypers

206 possible by the successful isolation of a M. smegmatis mutant strain mc(2)155, whose efficient plasmi

207 We identified a Mycobacterium smegmatis mutant, named FUEL (which stands for folate ut

208 We isolated 27 Mycobacterium smegmatis mutants that were hypersusceptible to Ub2.

209 Here we report that Mycobacterium smegmatis NucS/EndoMS, a putative endonuclease with no s

210 mosomal DNA between strains of Mycobacterium smegmatis occurs by a novel mechanism.

211 efficient DNA transfer between strains of M. smegmatis occurs in a mixed biofilm and that the process

212 a GFP reporter system, whether Mycobacterium smegmatis OhrR has the ability to sense and respond to i

213 hagocytosis and intracellular survival of M. smegmatis only in the absence of lysozyme but not under

214 ant are complemented by the expression of M. smegmatis or M. tuberculosis MmpL11, suggesting that Mmp

215 reporter proteins in wild-type Mycobacterium smegmatis or Mycobacterium tuberculosis.

216 inflammasome activation induced by either M. smegmatis or transfected dsDNA.

217 in M. smegmatis and M. tuberculosis, the M. smegmatis oriC is not MtrA-target.

218 bed of microscale silica beads to filter M. smegmatis out of the suspension.

219 selectively binds to M. tuberculosis and M. smegmatis peptidoglycans.

220 Unexpectedly, although the M. smegmatis phenotype was unaffected by the lack of manno-

221 We present the crystal structure of M. smegmatis PhnF at 1.8-A resolution, showing a homodimer

222 The full-length (763-aa) M. smegmatis PNPase is a homotrimeric enzyme with Mg(2+)*PO

223 nd DNA modifying activities of Mycobacterium smegmatis PNPase.

224 ate strands through a modified Mycobacterium smegmatis porin A (M2MspA) nanopore under control of phi

225 s such as alpha-haemolysin and Mycobacterium smegmatis porin A (MspA) can be used to sequence long st

226 neered biological protein pore Mycobacterium smegmatis porin A (MspA) to detect and map 5-methylcytos

227 tated form of the protein pore Mycobacterium smegmatis porin A (MspA) with phi29 DNA polymerase (DNAP

228 d DNA-NeutrAvidin complex in a Mycobacterium smegmatis porin A nanopore.

229 usion constant of DNA inside a Mycobacterium smegmatis porin A pore were determined to evaluate the t

230 current through the engineered Mycobacterium smegmatis porin A, MspA, has the ability to distinguish

231 the permeability defects of a Mycobacterium smegmatis porin mutant to glucose, serine and glycerol,

232 ne uptake across the outer membrane in an M. smegmatis porin mutant.

233 Mycobacterium smegmatis possesses two such transporters, the widely di

234 a large neutral LM (TB-LM); in contrast, M. smegmatis produces a smaller linear acidic LM (SmegLM) w

235 ty of phages of a common host, Mycobacterium smegmatis, provides a higher resolution of the phage pop

236 of RMPs in both reactions with Mycobacterium smegmatis RecO (MsRecO) and demonstrated that MsRecO int

237 Overexpression of oxyS in M. smegmatis reduced transcription of the ahpCD genes, whic

238 onstrate that RoxY and OxyS contribute to M. smegmatis resistance to oxidative stress.

239 ately 40- and 10-fold slower than that of M. smegmatis, respectively, which is consistent with the sl

240 n of the ortholog of Rv3789 in Mycobacterium smegmatis resulted in a reduction of the arabinose conte

241 lated, inactive form of MtrA in wild-type M. smegmatis resulted in phenotypes similar to those of lpq

242 letion of MSMEG_6281 (Ami1) in Mycobacterium smegmatis resulted in the formation of cellular chains,

243 Here, we identify and characterize M. smegmatis RqlH, a RecQ-like helicase with a distinctive

244 allowed complete phenotypic silencing of M. smegmatis secA1 with chromosomally integrated tetR genes

245 pathogenic model mycobacterium Mycobacterium smegmatis, SecA1 is essential for protein export and is

246 Here, we identify and characterize M. smegmatis SftH, a superfamily II helicase with a distinc

247 Antimycobacterial drug-treated M. smegmatis showed significant decreased in Ag85 antigen p

248 B-LM), but not from avirulent Myocobacterium smegmatis (SmegLM), is a potent inhibitor of TNF biosynt

249 ss mycolates on the surface of Mycobacterium smegmatis spheroplasts, allowing us to monitor flipping

250 vity against Escherichia coli, Mycobacterium smegmatis, Staphylococcus aureus and Staphylococcus simu

251 f polD1, polD2, or both from a Mycobacterium smegmatis strain carrying an inactivating mutation in Li

252 It was observed that M. smegmatis strains bearing the pohr-gfpuv fusion construc

253 ompared with wild type and vector control M. smegmatis strains.

254 rR in defense against oxidative stress in M. smegmatis, strains lacking the expression of these prote

255 hree different Actinobacteria (Mycobacterium smegmatis, Streptomyces lividans, and Rhodococcus jostii

256 Analysis of Mycobacterium smegmatis subcellular fractions and spheroplasts showed

257 hat BCG can reduce autophagy responses to M. smegmatis suggesting that specific mechanisms are used b

258 nt in Mtb and did not occur in Mycobacterium smegmatis, suggesting that V-58-mediated growth inhibiti

259 naturally occurring polymorphic NucS in a M. smegmatis surrogate model, suggests the existence of M.

260 coding ribosomal components in Mycobacterium smegmatis that confer resistance to several structurally

261 Mycobacterium tuberculosis and Mycobacterium smegmatis that has evolved independently from the previo

262 se-independent NHEJ pathway in Mycobacterium smegmatis that requires the ATP-dependent DNA ligase Lig

263 d levels were shown to be undetectable in M. smegmatis, the bound lipoyl residues of DlaT are the lik

264 In the nonpathogen Mycobacterium smegmatis, the ESX-1 T7SS plays a role in conjugation, a

265 In M. smegmatis, the esx-3 locus behaved like other iron-regul

266 However, when expressed in Mycobacterium smegmatis, the Rv0348 transcripts were significantly res

267 -3 expression in both M. tuberculosis and M. smegmatis, there is a significant difference in the dyna

268 y against Escherichia coli and Mycobacterium smegmatis, they proved to be highly potent inhibitors of

269 In M. smegmatis this coincided with up-regulation of the first

270 ession of nfnB resulted in sensitivity of M. smegmatis to 3.

271 in the intrinsic resistance of Mycobacterium smegmatis to a variety of stresses including the genotox

272 9R) of the model mycobacterium Mycobacterium smegmatis to better understand the pathway used by SecA2

273 g the spectrum of responses of Mycobacterium smegmatis to challenge with rifampicin.

274 required coadministration with Mycobacterium smegmatis to induce IL-1beta production and significant

275 li, Staphylococcus aureus, and Mycobacterium smegmatis to quinolone antibiotics.

276 For M. smegmatis TopoI-CTD, a 27-amino-acid tail that is rich i

277 conjugal recipient activity in Mycobacterium smegmatis Transcription of esx4 genes in the recipient r

278 e oxygen species production in Mycobacterium smegmatis treated with CFZ and a CFZ analog as well as e

279 r impact on gene expression in Mycobacterium smegmatis under hypochlorite stress.

280 phism on macrophage sensing of Mycobacterium smegmatis Upon infection with M. smegmatis, macrophages

281 n and menadione, whereas an fgd mutant of M. smegmatis used G6P less well under such conditions.

282 Importantly, MTHFS also affected M. smegmatis utilization of monoglutamylated 5-methyltetrah

283 The growth of M. smegmatis was also inhibited by high concentrations of R

284 monosodium urate crystals and Mycobacterium smegmatis was effective at delaying the growth of s.c. B

285 In the absence of MceG, M. smegmatis was not able to utilize cholesterol or phytost

286 The enzyme Msd from Mycobacterium smegmatis was taken as a representative candidate from a

287 the exochelin MS, the main siderophore of M. smegmatis, was not affected by the lack of porins, indic

288 tic resistance determinants in Mycobacterium smegmatis, we identified a multidrug-sensitive mutant wi

289 379 extracellular compounds of Mycobacterium smegmatis were deconvoluted with a genome-scale metaboli

290 apable of complementing LAM production in M. smegmatis were not viable in M. tuberculosis, supporting

291 ete the NCgl2760 orthologue in Mycobacterium smegmatis were unsuccessful, consistent with previous st

292 glycosyltransferase mutants of Mycobacterium smegmatis were used here to investigate these questions.

293 ired cell wall localization in Mycobacterium smegmatis, whereas mPDE-4A behaved similarly as wild typ

294 ive cluster ligand Asp13 (by analogy with M. smegmatis WhiB2) was not.

295 g each of the genes of the mce4 operon of M. smegmatis, which mediates the transport of cholesterol.

296 of Ohr expression was also noticed in an M. smegmatis wild-type strain (MSWt) induced with cumene hy

297 ounds, inhibited the growth of Mycobacterium smegmatis with an MIC80 value of 2 mug/mL.

298 from Aspergillus fumigatus and Mycobacterium smegmatis with K(d) values of 2.1 +/- 0.2 and 4.0 +/- 0.

299 000 V/cm field intensity was used to lyse M. smegmatis with long pulses (i.e., up to 30 pulses that w

300 Two other M. smegmatis Y-family polymerases, DinB1 and DinB3, are cha