ライフサイエンスコーパス: smegmatis

1 termined against Mycobacterium smegmatis (M. smegmatis).

2 second (p)ppGpp synthetase in Mycobacterium smegmatis.

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

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

5 including the closely related Mycobacterium smegmatis.

6 ed, and compared 627 phages of Mycobacterium smegmatis.

7 ts ortholog from nonpathogenic Mycobacterium smegmatis.

8 xpressed in the surrogate host Mycobacterium smegmatis.

9 lude the fast-growing organism Mycobacterium smegmatis.

10 ortant peroxide stress response system in M. smegmatis.

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

12 m in both Escherichia coli and Mycobacterium smegmatis.

13 ansporter activity in M. tuberculosis and M. smegmatis.

14 eprae SodC (rSodC) produced in Mycobacterium smegmatis.

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

16 -glutamate for peptidoglycan synthesis in M. smegmatis.

17 erium tuberculosis, but not in Mycobacterium smegmatis.

18 in the fast-growing surrogate, Mycobacterium smegmatis.

19 d the inner membrane lipids of Mycobacterium smegmatis.

20 at determines conjugal mating identity in M. smegmatis.

21 rculosis, Escherichia coli and Mycobacterium smegmatis.

22 sis and its avirulent relative Mycobacterium smegmatis.

23 ocalizations in the related non-pathogen, M. smegmatis.

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

25 of lipids in the microorganism Mycobacterium smegmatis.

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

27 proteins of the model organism Mycobacterium smegmatis.

28 Mycobacterium tuberculosis and Mycobacterium smegmatis.

29 al role of the CtpD protein of Mycobacterium smegmatis.

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

31 sis and its avirulent relative Mycobacterium smegmatis.

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

33 gene cluster ortholog found in Mycobacterium smegmatis.

34 cell, and cell pole regions in Mycobacterium smegmatis.

35 els of rifampicin tolerance in Mycobacterium smegmatis.

36 type VII secretion system from Mycobacterium smegmatis.

37 romosome of the model organism Mycobacterium smegmatis.

38 L1 was required for biofilm maturation in M. smegmatis.

39 terized the MceG orthologue of Mycobacterium smegmatis.

40 of cytokines in macrophages infected with M. smegmatis.

41 ress beta-lactam resistance in Mycobacterium smegmatis.

42 bility to impair the growth of Mycobacterium smegmatis.

43 tion of antioxidant defense mechanisms in M. smegmatis.

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

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

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

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

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

49 n of the SucT-encoding gene in Mycobacterium smegmatis abolished AG and LAM succinylation and altered

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

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

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

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

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

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

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

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

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

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

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

61 lored the role of this USP (USP(4207)) in M. smegmatis and found that its gene is present in an opero

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

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

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

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

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

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

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

69 Mycobacterium smegmatis and Mycobacterium kansasii were used as models

70 In contrast, Mycobacterium smegmatis and Mycobacterium tuberculosis accumulate dete

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

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

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

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

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

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

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

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

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

80 biofilm formation in M. tuberculosis and M. smegmatis, and non-replicating persistence in M. tubercu

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

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

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

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

85 e cellular function of HspX in Mycobacterium smegmatis as both a pro-aggregase and polar sortase.

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

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

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

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

90 LprE (Mtb) expressing M. tuberculosis and M. smegmatis because of a surge in the expression of cathel

91 and whose transcript levels increased in M. smegmatis biofilms along with that of USP(4207), suggest

92 Growth of Mycobacterium smegmatis biofilms requires multiple factors including a

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

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

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

96 edox cofactor that oxidizes NADH bound by M. smegmatis carveol dehydrogenase (MsCDH) and can be used

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

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

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

100 xpressed heterologously in live yeast and M. smegmatis cells.

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

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

103 ing a conditional knockout constructed in M. smegmatis confirm the essentiality of the putative activ

104 Their expression in Mycobacterium smegmatis confirmed that these PE/PPE proteins inhibit a

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

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

107 Mycobacterium smegmatis contains 6 homologous mce (mammalian cell entr

108 Mycobacterium smegmatis contains three hemerythrin-like proteins, MSME

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

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

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

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

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

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

115 tin auxotrophy, and addition of biotin to M. smegmatis cultures repressed tam gene transcription.

116 single-cell Raman microscopy, Mycobacterium smegmatis cultures were fixed using a new fast and gentl

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

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

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

120 Notably, nonpathogenic Mycobacterium smegmatis did not increase MDR1 expression, indicating a

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

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

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

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

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

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

127 ectron microscopy structure of Mycobacterium smegmatis EmbB, providing insights on substrate binding

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

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

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

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

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

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

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

135 Mycobacterium tuberculosis and M. smegmatis form drug-tolerant biofilms through dedicated

136 s of Rv1747 and its homolog in Mycobacterium smegmatis form liquid-like condensates as a function of

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

138 We report that the Mycobacterium smegmatis gene annotated as encoding Tam, an O-methyltra

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

140 The impacts on M. smegmatis growth range from mild to severe, but many cau

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

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

143 The soil saprophyte Mycobacterium smegmatis has two such [NiFe] hydrogenases, designated H

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

145 We also show that unlike the M. smegmatis homologue which was not essential for growth,

146 al expression of LprE (Mtb) in Mycobacterium smegmatis improved bacterial survival.

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

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

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

150 ally Staphylococcus aureus and Mycobacterium smegmatis, in a MscL-dependent manner.

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

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

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

154 hes, we established that PE of Mycobacterium smegmatis is exported to the cell envelope following cle

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

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

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

158 a gene of unknown function in Mycobacterium smegmatis, is up-regulated in response to hypoxia and re

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

160 10 uM) are required to observe Mycobacterium smegmatis killing.

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

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

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

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

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

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

167 ria, these findings obtained with PE from M. smegmatis may offer clues to glycolipid formation in M.

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

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

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

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

172 ssed in the heterologous host, Mycobacterium smegmatis mc(2)-155.

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

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

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

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

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

178 es for ethanol assimilation in Mycobacterium smegmatis mc(2)155.

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

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

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

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

183 report the characterization of Mycobacterium smegmatis MmpL11.

184 report a crystal structure of Mycobacterium smegmatis MmpL3 at a resolution of 2.59 angstrom, reveal

185 nd to accommodate different inhibitors in M. smegmatis MmpL3.

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

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

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

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

190 tuted from IM and OM lipids in vitro from M. smegmatis (Msm) underscored by their lipid packing and l

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

192 n-pathogenic mycobacterial model organism M. smegmatis (Msmeg), to identify genes required for sidero

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

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

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

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

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

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

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

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

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

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

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

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

205 tase reduced the survival of phagocytosed M. smegmatis or M. tuberculosis D. discoideum cells lacking

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

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

208 Corynebacterium glutamicum and Mycobacterium smegmatis, organisms that serve as models of Mycobacteri

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

210 However, for the M. smegmatis orthologues, results from isothermal titration

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

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

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

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

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

216 nd DNA modifying activities of Mycobacterium smegmatis PNPase.

217 eased killing of phagocytosed E. coli and M. smegmatis Polyphosphate inhibited phagosome acidificatio

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

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

220 frequency of 200 Hz, across a Mycobacterium smegmatis porin A (MspA) nanopore, thus changing how the

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

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

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

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

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

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

227 Mycobacterium smegmatis possesses two such transporters, the widely di

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

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

230 g expression of polyphosphate kinase 1 in M. smegmatis reduced extracellular polyphosphate and reduce

231 Why does M. smegmatis require two hydrogenases with a seemingly simi

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

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

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

235 , as well as the nonpathogenic Mycobacterium smegmatis, results in hypersensitivity to the macrolide-

236 h recombinant HBHA produced in Mycobacterium smegmatis (rHBHA-Ms), we could link antigenic difference

237 cture of a complex between the Mycobacterium smegmatis RNAP and HelD.

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

239 tron microscopy structure of a Mycobacterium smegmatis Sdh, which forms a trimer.

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

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

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

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

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

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

246 l assays with spheroplasts derived from a M. smegmatis strain lacking the endogenous mmpL3 gene but h

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

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

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

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

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

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

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

254 lemented biotin-independent growth of the M. smegmatis tam deletion mutant strain.

255 The M. smegmatis Tam functionally replaced Escherichia coli Bio

256 Moreover, deletion of the M. smegmatis tam gene resulted in biotin auxotrophy, and ad

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

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

259 previously identified a USP in Mycobacterium smegmatis that is a product of the msmeg_4207 gene and i

260 trehalose synthase:maltokinase complex in M. smegmatis that offers critical insights into capsule ass

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

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

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

264 Here, we show that in Mycobacterium smegmatis, the small heat shock protein HspX plays a cri

265 -3 expression in both M. tuberculosis and M. smegmatis, there is a significant difference in the dyna

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

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

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

269 9R) of the model mycobacterium Mycobacterium smegmatis to better understand the pathway used by SecA2

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

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

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

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

274 mall ssDNA oligonucleotides to Mycobacterium smegmatis topoisomerase I with progressive C-terminal de

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

276 t the crystal structure of the Mycobacterium smegmatis TreS:Pep2 complex, containing trehalose syntha

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

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

279 nses to cysteine limitation in Mycobacterium smegmatis using mass spectrometry.

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

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

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

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

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

285 and genome-wide repair map of Mycobacterium smegmatis We find that M. smegmatis, which possesses hom

286 379 extracellular compounds of Mycobacterium smegmatis were deconvoluted with a genome-scale metaboli

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

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

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

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

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

292 thase has been determined from Mycobacterium smegmatis which hydrolyzes ATP very poorly.

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

294 p of Mycobacterium smegmatis We find that M. smegmatis, which possesses homologs of the Escherichia c

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

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

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

298 000 V/cm field intensity was used to lyse M. smegmatis with long pulses (i.e., up to 30 pulses that w

299 When deployed in Mycobacterium smegmatis with quantitative proteomics, this strategy en

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