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 CAMLP, expressed in Escherichia coli, exhib

3 M. smegmatis growing on specific solid media was also tr

4 M. smegmatis strains that overexpressed replication prot

5 M. smegmatis surface motility is similarly dependent on

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

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

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

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

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

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

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

13 Additionally, M. smegmatis-infected macrophages produced significantly

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

40 mid transfer was also shown to occur between M. smegmatis strains.

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

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

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

44 e, Rv0834c, in a pH-dependent manner in both M. smegmatis and M. tuberculosis.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

64 it was coded by a gene in the databases for M. smegmatis and M. tuberculosis previously designated a

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

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

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

68 ucture of arylamine N-acetyltransferase from M. smegmatis at a resolution of 1.7 A as a model for the

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

70 Deletion of CysH from M. smegmatis afforded a cysteine and methionine auxotrop

71 Although the original enzyme from M. smegmatis was greatly stimulated in its utilization o

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

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

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

75 The purified enzyme, either isolated from M. smegmatis, or expressed in E. coli, rapidly dephospho

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

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

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

79 Like the enzyme originally purified from M. smegmatis, the recombinant enzyme is an unusual glyco

80 Furthermore, M. smegmatis ald null mutants were constructed by target

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

85 000-based extrachromosomal plasmids is 23 in M. smegmatis as determined by quantitative real-time PCR

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

101 fadD28 and mas promoters were functional in M. smegmatis, at approximately two- and sixfold-higher l

102 larger protein was coded by the same gene in M. smegmatis but included an eight amino acid N-terminal

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

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

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

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

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

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

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

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

111 that determines conjugal mating identity in M. smegmatis.

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

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

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

115 duction of antioxidant defense mechanisms in M. smegmatis.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

131 ologous sequences or inactivation of recA in M. smegmatis.

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

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

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

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

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

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

138 important peroxide stress response system in M. smegmatis.

139 her, these results show that DNA transfer in M. smegmatis occurs by a mechanism different from that o

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

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

142 pitation of PhoA from [(14)C]acetate-labeled M. smegmatis cell lysates demonstrated that this phospha

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

144 0-8000 V/cm field intensity was used to lyse M. smegmatis with long pulses (i.e., up to 30 pulses tha

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

166 These inhibitors block the growth of M. smegmatis.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

201 extracellular and intracellular survival of M. smegmatis.

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

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

204 Streptomyces, followed by transformation of M. smegmatis.

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

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

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

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

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

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

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

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

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

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

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

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

217 calcium promotes oligomerization of purified M. smegmatis CAMLP.

218 Interestingly, the putative M. smegmatis PhoA has a hydrophobic N-terminal domain wh

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

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

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

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

223 effect on the immunogenicity of recombinant M. smegmatis.

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

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

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

227 determined against Mycobacterium smegmatis (M. smegmatis).

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

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

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

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

232 DNA sequence analysis revealed that M. smegmatis does indeed have a phoA gene that shows hig

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

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

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

236 The M. smegmatis MSMEG_0023 crgA double mutant strain showed

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

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

239 The M. smegmatis phoA gene was shown to be induced by phosph

240 The M. smegmatis PhoA was demonstrated to be an exported pro

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

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

243 In addition, the M. smegmatis vacuole harboring TM4 fuses with the M. avi

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

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

246 In summary, the phenotypes displayed by the M. smegmatis ald mutants suggest that Ald plays an impor

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

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

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

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

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

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

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

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

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

259 0.2 proteins, can complement for loss of the M. smegmatis cpn60.1 gene.

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

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

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

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

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

265 Based on these peptides, the M. smegmatis gene for TPP was cloned and expressed in E.

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

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

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

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

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

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

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

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

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

275 not kasA, confers INH and ETH resistance to M. smegmatis, M. bovis BCG and M. tuberculosis.

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

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

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

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

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

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

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

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

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

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

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

287 1 mutant was distinct from that by wild-type M. smegmatis.

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

289 Transformation frequencies were higher when M. smegmatis was co-cultivated with plasmid-free Strepto

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

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

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

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

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

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

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

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

298 ulosis-infected, RAW 264.7 macrophages, with M. smegmatis transiently infected with TM4, resulted in

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

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