ライフサイエンスコーパス: M. smegmatis

1 M. smegmatis and other nonpathogenic mycobacteria are pr

2 M. smegmatis strains that overexpressed replication prot

3 M. smegmatis surface motility is similarly dependent on

4 M. smegmatis, therefore, represents a powerful system to

5 A M. smegmatis DeltacrgA strain exhibited a bulged cell mo

6 Similar phenotypes were observed for a M. smegmatis mutant lacking the homolog Ms3747, demonstr

7 onal assays with spheroplasts derived from a M. smegmatis strain lacking the endogenous mmpL3 gene bu

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

9 Complementation studies of a M. smegmatis glgE mutant strain with these GlgE derivati

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

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

12 Additionally, M. smegmatis-infected macrophages produced significantly

13 Importantly, MTHFS also affected M. smegmatis utilization of monoglutamylated 5-methyltet

14 An M. smegmatis Delta recA Delta ku double mutant has no ap

15 An M. smegmatis mutant strain lacking the ctpD gene was hyp

16 oline uptake across the outer membrane in an M. smegmatis porin mutant.

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

18 We show here that an M. smegmatis Delta ponA2 mutant has an unusual antibioti

19 locus were rapidly lethal, infection with an M. smegmatis Deltaesx-3 mutant (here designated as the I

20 ncreased killing of phagocytosed E. coli and M. smegmatis Polyphosphate inhibited phagosome acidifica

21 sity (OD) from micro cultures of E. coli and M. smegmatis.

22 els, including M. bovis BCG, M. marinum, and M. smegmatis have significantly contributed to understan

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

24 n the vacuole of pathogenic mycobacteria and M. smegmatis.

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

26 differences of esx-3 in M. tuberculosis and M. smegmatis and demonstrate the importance of metal-dep

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

28 hat has been detected in M. tuberculosis and M. smegmatis cultures.

29 Thus, M. tuberculosis and M. smegmatis enzymes are interchangeable and do not cont

30 Mycobacterium tuberculosis and M. smegmatis form drug-tolerant biofilms through dedicat

31 n A selectively binds to M. tuberculosis and M. smegmatis peptidoglycans.

32 esults indicate that the M. tuberculosis and M. smegmatis RD1 regions are functionally equivalent and

33 in intergenic regions of M. tuberculosis and M. smegmatis respectively.

34 to biofilm formation in M. tuberculosis and M. smegmatis, and non-replicating persistence in M. tube

35 to the peptidoglycans in M. tuberculosis and M. smegmatis, the muramic acid residues of M. leprae pep

36 esx-3 expression in both M. tuberculosis and M. smegmatis, there is a significant difference in the d

37 transporter activity in M. tuberculosis and M. smegmatis.

38 ound impact on growth of M. tuberculosis and M. smegmatis.

39 n expressed heterologously in live yeast and M. smegmatis cells.

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

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

42 tuberculosis and M. avium or with avirulent M. smegmatis.

43 SecA2-dependent export are conserved between M. smegmatis and M. tuberculosis.

44 Despite the evolutionary distance between M. smegmatis and M. tuberculosis, the M. smegmatis Snm s

45 that are essential to eis expression in both M. smegmatis and M. tuberculosis H37Ra, including a regi

46 itivity to 2-deoxy-galactose (2-DOG) in both M. smegmatis and M. tuberculosis.

47 nation facilitating allelic exchange in both M. smegmatis and M. tuberculosis.

48 modulin/calmodulin kinase II pathway in both M. smegmatis- and M. avium-infected macrophages.

49 e redox cofactor that oxidizes NADH bound by M. smegmatis carveol dehydrogenase (MsCDH) and can be us

50 ered in the environmental niches occupied by M. smegmatis and other soil-dwelling mycobacteria.

51 e domains and the full-length Lysin A caused M. smegmatis cell lysis.

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

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

54 Here, we identify and characterize M. smegmatis SftH, a superfamily II helicase with a dist

55 ng this system, we constructed a conditional M. smegmatis knockdown mutant in which addition of anhyd

56 Consistently, M. smegmatis LigD null strains are entirely and selectiv

57 and immunoblotting of phagosomes containing M. smegmatis strains revealed that the phagosomes with t

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

59 s compared with wild type and vector control M. smegmatis strains.

60 vectored by fast-growing, readily destroyed M. smegmatis is processed and presented on MHC class I b

61 se the model BBB significantly more than did M. smegmatis (a nonpathogenic mycobacterium).

62 Why does M. smegmatis require two hydrogenases with a seemingly s

63 M2 inflammasome activation induced by either M. smegmatis or transfected dsDNA.

64 These are the first endogenous M. smegmatis proteins identified as dependent on SecA2 f

65 of macrophages infected with esxL-expressing M. smegmatis and mouse splenocytes led to down-regulatio

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

67 antly diminished promoter activity following M. smegmatis infection but not M. avium infection.

68 For M. smegmatis TopoI-CTD, a 27-amino-acid tail that is ric

69 uranose residue to galactan is essential for M. smegmatis viability.

70 A similar result was obtained for M. smegmatis that overexpressed endogenous alkaline phos

71 ase is not only an improved genetic tool for M. smegmatis, but can also be used in slow growing mycob

72 use of an endogenous endo-D-arabinanase from M. smegmatis, profiled, and sequenced directly by tandem

73 M. tuberculosis carrying FabG from M. smegmatis showed no phenotypic changes, and both the

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

75 Ado cleavage activities were identified from M. smegmatis cell extracts.

76 we also showed that the presence of P27 from M. smegmatis decreases the association of LAMP-3 with be

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

78 rase assay using a membrane preparation from M. smegmatis expressing Rv3792 and synthetic beta-d-Galf

79 entify a total of 901 distinct proteins from M. smegmatis over the course of 25 growth conditions, pr

80 stituted from IM and OM lipids in vitro from M. smegmatis (Msm) underscored by their lipid packing an

81 In M. smegmatis this coincided with up-regulation of the fi

82 In M. smegmatis, all four recombinant-overexpressed GS are

83 In M. smegmatis, the esx-3 locus behaved like other iron-re

84 cing expression of polyphosphate kinase 1 in M. smegmatis reduced extracellular polyphosphate and red

85 presence of nine acidic amino acids (16%) in M. smegmatis CAMLP, there is one putative calcium-bindin

86 000-based extrachromosomal plasmids is 23 in M. smegmatis as determined by quantitative real-time PCR

87 explored the role of this USP (USP(4207)) in M. smegmatis and found that its gene is present in an op

88 in (CREB) is significantly more activated in M. smegmatis-infected macrophages than in M. avium-infec

89 verexpression of either Rv2629 191 allele in M. smegmatis did not produce an increase in rifampin res

90 g establishment of the MtbESX-1 apparatus in M. smegmatis.

91 he trehalose synthase:maltokinase complex in M. smegmatis that offers critical insights into capsule

92 using a conditional knockout constructed in M. smegmatis confirm the essentiality of the putative ac

93 Overexpression of recombinant TopoI-CTD in M. smegmatis competed with the endogenous topoisomerase

94 . coelicolor whiB complemented the defect in M. smegmatis 628-53, indicating that these genes are tru

95 two M. tuberculosis genes, hspX and eis, in M. smegmatis in the presence and absence of rel(Msm).

96 Such substitutions, when engineered, in M. smegmatis enzyme caused the following.

97 treptomyces coelicolor whiB, is essential in M. smegmatis, and the conditionally complemented mutant

98 two proteins showed no obvious Tat export in M. smegmatis.

99 is cytoplasmic but the M. tb MS expressed in M. smegmatis localizes to the cell wall and enhances the

100 ropose that PyrR regulates pyr expression in M. smegmatis, other mycobacteria, and probably in numero

101 nhanced yellow fluorescent protein (EYFP) in M. smegmatis.

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

103 inase was increased by more than 100-fold in M. smegmatis.

104 inding in vitro and inhibit FtsX function in M. smegmatis.

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

106 s we were successful in deleting the gene in M. smegmatis.

107 ectly controls the expression of 83 genes in M. smegmatis, and 74 in M. tuberculosis.

108 s necessary for maximum expression of gfp in M. smegmatis and M. tuberculosis H37Ra, respectively.

109 ncement of stability for the modified GFP in M. smegmatis.

110 ant for Co(2)(+) and Ni(2)(+) homeostasis in M. smegmatis, and that M. tuberculosis CtpD orthologue c

111 Deletion of the Rv0008c homolog in M. smegmatis, MSMEG_0023, caused bulged cell poles, form

112 tivity, deletion of the Rv1459c homologue in M. smegmatis did not result in loss of mycobacterial LM/

113 that determines conjugal mating identity in M. smegmatis.

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

115 found to accommodate different inhibitors in M. smegmatis MmpL3.

116 studied the effects of depletion of KasA in M. smegmatis using the former strain as a reference.

117 covered that the inducer molecule of KstR in M. smegmatis mc(2)155 is not cholesterol but 3-oxo-4-cho

118 nd that the cellular concentration of LAM in M. smegmatis is selectively modulated with the growth ph

119 roEL1 was required for biofilm maturation in M. smegmatis.

120 duction of antioxidant defense mechanisms in M. smegmatis.

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

122 espite the near sequence identity of MtrA in M. smegmatis and M. tuberculosis, the M. smegmatis oriC

123 conjugation phenotype of the RD1 mutants in M. smegmatis.

124 n the time to generate unmarked mutations in M. smegmatis and M. tuberculosis.

125 e show that the Snm system is operational in M. smegmatis and that secretion of its homologous ESAT-6

126 MtmanB overexpression in M. smegmatis produced increased levels of LAM, lipomanna

127 Overexpression of oxyS in M. smegmatis reduced transcription of the ahpCD genes, w

128 Fe/Mn-superoxide dismutase, particularly in M. smegmatis.

129 tion of the cAMP/protein kinase A pathway in M. smegmatis-infected cells was required for the prolong

130 s required for each of the three pathways in M. smegmatis by allelic replacement.

131 M channels for the diffusion of phosphate in M. smegmatis.

132 incapable of complementing LAM production in M. smegmatis were not viable in M. tuberculosis, support

133 ere done to characterize the eis promoter in M. smegmatis and M. tuberculosis H37Ra.

134 lyzed all three hemerythrin-like proteins in M. smegmatis and our results identified and characterize

135 vergence of the hemerythrin-like proteins in M. smegmatis.

136 The stringent response plays a role in M. smegmatis cellular and colony formation that is sugge

137 Importantly, we show that Snm secretion in M. smegmatis requires genes that are homologous to those

138 Using a gene knockout strategy in M. smegmatis, we have also discovered four new gene prod

139 OhrR in defense against oxidative stress in M. smegmatis, strains lacking the expression of these pr

140 f D-glutamate for peptidoglycan synthesis in M. smegmatis.

141 are required for a functional TAT system in M. smegmatis.

142 important peroxide stress response system in M. smegmatis.

143 acid levels were shown to be undetectable in M. smegmatis, the bound lipoyl residues of DlaT are the

144 ial-fillable" powders of bacteria (including M. smegmatis and M. bovis BCG) can be produced.

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

146 0-8000 V/cm field intensity was used to lyse M. smegmatis with long pulses (i.e., up to 30 pulses tha

147 ants were in the mspA gene encoding the main M. smegmatis porin.

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

149 Moreover, M. smegmatis strains overexpressing Rep enhanced gene tr

150 g colonies of transposon (Tn611)-mutagenized M. smegmatis.

151 s, and the conditionally complemented mutant M. smegmatis 628-53 undergoes filamentation under nonper

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

153 is study, we show that one of these mutants, M. smegmatis strain PM440, utilizes lanthionine, an unus

154 ith propargylglycine suppressed clearance of M. smegmatis by macrophages and inhibited phagolysosomal

155 ximately 93% is sufficient to cause death of M. smegmatis.

156 porins resulted in a severe growth defect of M. smegmatis on low-phosphate plates.

157 Deletion of M. smegmatis MSMEG2785 resulted in altered growth and gl

158 mutant are complemented by the expression of M. smegmatis or M. tuberculosis MmpL11, suggesting that

159 Using cell-free extracts of M. smegmatis mc(2)155, little activity was obtained with

160 Gfp expression and fluorescence of M. smegmatis and M. tuberculosis strains with multiple i

161 t Ub2 treatment impairs membrane function of M. smegmatis and M. tuberculosis cells.

162 provided that pimB' is an essential gene of M. smegmatis.

163 The genome of M. smegmatis was analyzed with the TATFIND program, and

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

165 The growth of M. smegmatis was also inhibited by high concentrations o

166 serve as a sole carbon source for growth of M. smegmatis, indicate that MSH functions not only as a

167 cating that UvrD2 is essential for growth of M. smegmatis.

168 These inhibitors block the growth of M. smegmatis.

169 Inactivation of M. smegmatis MSMEG4250 by allelic exchange resulted in a

170 enes are expressed upon RedRock infection of M. smegmatis, but are downregulated once lysogeny is est

171 suggests that the lipid II intermediates of M. smegmatis are substrates for a variety of enzymes tha

172 ller molecular size (approximately 6 kDa) of M. smegmatis CAMLP.

173 e in the export of active beta-lactamases of M. smegmatis (BlaS) and M. tuberculosis (BlaC), both of

174 hange at the chromosomal MSMEG_6386 locus of M. smegmatis could only be achieved in the presence of a

175 oli lysates containing Rv3230c to lysates of M. smegmatis expressing DesA3 gave strong conversion of

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

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

178 ucose uptake and growth of a porin mutant of M. smegmatis.

179 DeltatatA and DeltatatC deletion mutants of M. smegmatis, which demonstrated that tatA and tatC enco

180 We concluded that the OM of M. smegmatis represents a permeability barrier for phosp

181 ting each of the genes of the mce4 operon of M. smegmatis, which mediates the transport of cholestero

182 s shown by the 10-fold lower permeability of M. smegmatis for phosphate compared to that for glucose.

183 at complement the filamentation phenotype of M. smegmatis 628-53 following inducer withdrawal.

184 tem has a direct effect on the physiology of M. smegmatis and homologs of the TAT proteins are also p

185 ) and the beta' subunit of RNA polymerase of M. smegmatis in the absence of DNA.

186 etion pathway, we analyzed the main porin of M. smegmatis, MspA.

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

188 fusions and resembled sigma(A) promoters of M. smegmatis.

189 ntercalating in DNA and impaired recovery of M. smegmatis from UV irradiation.

190 creen for their ability to delay recovery of M. smegmatis from UV irradiation.

191 sites in the phnD-phnF intergenic region of M. smegmatis has allowed us to propose a quantitative mo

192 as responsible for the natural resistance of M. smegmatis against 3.

193 xpression of nfnB resulted in sensitivity of M. smegmatis to 3.

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

195 and allowed complete phenotypic silencing of M. smegmatis secA1 with chromosomally integrated tetR ge

196 The msrA mutant strain of M. smegmatis exhibited significantly reduced intracellul

197 In addition, the msrA mutant strain of M. smegmatis was observed to be more sensitive to hydrop

198 at efficient DNA transfer between strains of M. smegmatis occurs in a mixed biofilm and that the proc

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

200 The study of M. smegmatis is expected to shed light on mechanisms of

201 e pair elevated the invasion and survival of M. smegmatis 2-3-fold in secondary cell lines in the pre

202 d phagocytosis and intracellular survival of M. smegmatis only in the absence of lysozyme but not und

203 extracellular and intracellular survival of M. smegmatis.

204 int mutant, we showed that susceptibility of M. smegmatis to Ub2 was independent of MspA channel acti

205 ximately 40- and 10-fold slower than that of M. smegmatis, respectively, which is consistent with the

206 , isolated following vancomycin treatment of M. smegmatis, consisted of the N-glycolyl derivative onl

207 The use of M. smegmatis as a tool for studying the mycobacterial st

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

209 re also identified in M. tuberculosis and/or M. smegmatis.

210 macrophages infected with either M. avium or M. smegmatis.

211 contrast, LPS, monosodium urate crystals, or M. smegmatis alone had no activity.

212 non-pathogenic mycobacterial model organism M. smegmatis (Msmeg), to identify genes required for sid

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

214 l localizations in the related non-pathogen, M. smegmatis.

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

216 phatase reduced the survival of phagocytosed M. smegmatis or M. tuberculosis D. discoideum cells lack

217 -fast bacilli, while in the stationary phase M. smegmatis lost the characteristic rod shape and devel

218 from M. fortuitum, M. scofulaceum, M. phlei, M. smegmatis, and M. gordonae.

219 modulate two seemingly disparate processes, M. smegmatis DNA transfer and M. tuberculosis virulence.

220 d (iii) RnhB and RnhA collaborate to protect M. smegmatis against oxidative damage in stationary phas

221 have successfully overexpressed and purified M. smegmatis EgtE enzyme and evaluated its activities un

222 turation of dendritic cells, but recombinant M. smegmatis infection led to a greater degree of dendri

223 Antigen from recombinant M. smegmatis was processed and presented as OVA(257-264)

224 Recombinant M. bovis BCG but not recombinant M. smegmatis conferred protection to mice challenged wit

225 Whole cell digestion of recombinant M. smegmatis with proteinase K showed that Rv1698 is sur

226 effect on the immunogenicity of recombinant M. smegmatis.

227 Immunization of mice with recombinant M. smegmatis led to the expansion of major histocompatib

228 strain deficient for the stringent response (M. smegmatis Delta rel(Msm) strain) and is not a reversi

229 ingle-cell level in Mycobacterium smegmatis (M. smegmatis) and Mycobacterium bovis Bacillus Calmette-

230 determined against Mycobacterium smegmatis (M. smegmatis).

231 Surprisingly, M. smegmatis has three paralogs of SMC proteins: EptC an

232 not provide redundant capabilities and that M. smegmatis, in contrast with Mycobacterium tuberculosi

233 map of Mycobacterium smegmatis We find that M. smegmatis, which possesses homologs of the Escherichi

234 It was observed that M. smegmatis strains bearing the pohr-gfpuv fusion const

235 We showed previously that M. smegmatis lacking MmpL11 has reduced membrane permeab

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

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

238 These results show for the first time that M. smegmatis regulates porin gene expression to optimize

239 The M. smegmatis MSMEG_0023 crgA double mutant strain showed

240 The M. smegmatis mtrB mutant was filamentous, defective for

241 The M. smegmatis mutant is devoid of UDP-N-acetylmuramic aci

242 The M. smegmatis Tam functionally replaced Escherichia coli

243 The M. smegmatis Ub2-resistant mutants were more resistant t

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

245 Although the M. smegmatis genome sequence is not yet completed, we us

246 Unexpectedly, although the M. smegmatis phenotype was unaffected by the lack of man

247 We found that biofilm formation by the M. smegmatis mmpL11 mutant was distinct from that by wil

248 Plasmids containing the M. smegmatis pyr promoter-leader region translationally

249 Attempts to disrupt the M. smegmatis uvrD2 gene were unsuccessful unless a secon

250 However, for the M. smegmatis orthologues, results from isothermal titrat

251 ions to map a donor-determining locus in the M. smegmatis chromosome using genetic linkage analysis.

252 and ESX-1 secretion, first described in the M. smegmatis donor.

253 eptides, the treS gene was identified in the M. smegmatis genome sequence, and was cloned and express

254 creen identifies novel non-esx-1 loci in the M. smegmatis genome that are required for both DNA trans

255 Instead, the M. smegmatis Ub2-resistant mutants shared a common pheno

256 The LAM content of the M. smegmatis cell wall was dramatically reduced as the b

257 s further underline the unique nature of the M. smegmatis chromosomal transfer system.

258 , the mutations map to a 25-kb region of the M. smegmatis chromosome that is syntenous with the RD1 r

259 ibe the capture and deletion of 25 kb of the M. smegmatis chromosome, and targeted-allele exchange of

260 0.2 proteins, can complement for loss of the M. smegmatis cpn60.1 gene.

261 Complementation of the M. smegmatis deletion mutant was fully restored to a wil

262 t herein the further characterization of the M. smegmatis mmpL11 mutant and identification of the Mmp

263 Phenotypes of the M. smegmatis mmpL11 mutant are complemented by the expre

264 complemented the permeability defect of the M. smegmatis porin mutant for glucose.

265 omplemented biotin-independent growth of the M. smegmatis tam deletion mutant strain.

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

267 Microarray analysis of the M. smegmatis transcriptome shows that iron-responsive ge

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

269 etween M. smegmatis and M. tuberculosis, the M. smegmatis Snm system can secrete the M. tuberculosis

270 We also show that unlike the M. smegmatis homologue which was not essential for growt

271 This M. smegmatis-induced cAMP production was also dependent

272 lipid moiety is decaprenyl phosphate; thus, M. smegmatis is the first bacterium reported to utilize

273 yl-radical scavenger thiourea, when added to M. smegmatis cultures maintained at high DO levels, resc

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

275 crophages infected with M. avium compared to M. smegmatis showed diminished TNF-alpha and NOS2 promot

276 demonstrate that RoxY and OxyS contribute to M. smegmatis resistance to oxidative stress.

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

278 ed, rapidly growing mycobacterium related to M. smegmatis, was isolated both from the abdominal wall

279 s that BCG can reduce autophagy responses to M. smegmatis suggesting that specific mechanisms are use

280 t overexpression of the proteins is toxic to M. smegmatis, although whether this toxicity and the ass

281 Antimycobacterial drug-treated M. smegmatis showed significant decreased in Ag85 antige

282 ursors, whereas those from similarly treated M. smegmatis consisted of a mixture of N-glycolylated an

283 ed as a surrogate for virulent tuberculosis; M. smegmatis (MSm) is utilized as a near-neighbor confou

284 In crosses using two M. smegmatis donors, we show that wild-type cells can su

285 stance to ethidium bromide in both wild-type M. smegmatis and the complemented mutant, suggesting tha

286 e lsr2 gene was inactivated in the wild-type M. smegmatis mc(2)155 strain by allelic replacement to c

287 orylated, inactive form of MtrA in wild-type M. smegmatis resulted in phenotypes similar to those of

288 t mutants were more resistant than wild-type M. smegmatis to this damage.

289 spC was twofold lower than that by wild-type M. smegmatis.

290 1 mutant was distinct from that by wild-type M. smegmatis.

291 ared the efficiencies of gene transfer using M. smegmatis or BCG containing chromosomal insertions or

292 native cluster ligand Asp13 (by analogy with M. smegmatis WhiB2) was not.

293 F-kappaB promoter activities associated with M. smegmatis-infected macrophages are responsible, at le

294 However, in macrophages infected with M. smegmatis but not M. avium, we observed a marked incr

295 Finally, in macrophages infected with M. smegmatis compared with M. avium, we observed enhance

296 f cPKC and PI3K in macrophages infected with M. smegmatis compared with M. avium.

297 d transfer to eukaryotic cells infected with M. smegmatis hyperconjugation mutants.

298 on of cytokines in macrophages infected with M. smegmatis.

299 Mycobacterium smegmatis Upon infection with M. smegmatis, macrophages from knock-in mice harboring R

300 derophores under low-iron conditions than wt M. smegmatis.

301 utant was reduced compared to wild-type (wt) M. smegmatis.