scholarly journals GldI Is a Lipoprotein That Is Required for Flavobacterium johnsoniae Gliding Motility and Chitin Utilization

2004 ◽  
Vol 186 (8) ◽  
pp. 2295-2302 ◽  
Author(s):  
Mark J. McBride ◽  
Timothy F. Braun
Keyword(s):  
Cell Envelope ◽  
Gliding Motility ◽  
Wild Type ◽  
Fk506 Binding Protein ◽  
Flavobacterium Johnsoniae ◽  
Acid Protein ◽  
Phage Sensitivity ◽  
Colony Spreading ◽  
Protein Components ◽  
Amino Acid Protein

ABSTRACT Cells of Flavobacterium johnsoniae glide rapidly over surfaces by an unknown mechanism. Seven genes (gldA, gldB, gldD, gldF, gldG, gldH, and ftsX) that are required for gliding motility have been described. Complementation of the nonmotile mutants UW102-41, UW102-85, and UW102-92 identified another gene, gldI, that is required for gliding motility. gldI mutants formed nonspreading colonies, and individual cells were completely nonmotile. They were also resistant to bacteriophages that infect wild-type cells, and they failed to digest chitin. Introduction of wild-type gldI on a plasmid restored colony spreading, cell motility, phage sensitivity, and the ability to digest chitin to the gldI mutants. gldI encodes a predicted 199-amino-acid protein that localized to the membrane fraction. Labeling studies with [3H]palmitate indicated that GldI is a lipoprotein. GldI is similar to peptidyl-prolyl cis/trans-isomerases of the FK506-binding protein family and may be involved in folding cell envelope protein components of the motility machinery.

scholarly journals Flavobacterium johnsoniae GldH Is a Lipoprotein That Is Required for Gliding Motility and Chitin Utilization

2003 ◽  
Vol 185 (22) ◽  
pp. 6648-6657 ◽  
Author(s):  
Mark J. McBride ◽  
Timothy F. Braun ◽  
Jessica L. Brust
Keyword(s):  
Amino Acid ◽  
Cell Movement ◽  
Gliding Motility ◽  
Wild Type ◽  
Cytophaga Hutchinsonii ◽  
Flavobacterium Johnsoniae ◽  
Acid Protein ◽  
Latex Spheres ◽  
Phage Sensitivity ◽  
Colony Spreading

ABSTRACT Cells of Flavobacterium johnsoniae move rapidly over surfaces by gliding motility. The mechanism of this form of motility is not known. Six genes (gldA, gldB, gldD, gldF, gldG, and ftsX) that are required for gliding have been described. Tn4351 mutagenesis was used to identify another gene, gldH, which is required for cell movement. GldH mutants formed nonspreading colonies, and individual cells lacked the cell movements and ability to propel latex spheres along their surfaces that are characteristic of wild-type cells. gldH mutants also failed to digest chitin and were resistant to bacteriophages that infect wild-type cells. Introduction of pMM293, which carries wild-type gldH, restored to the gldH mutants colony spreading, cell motility, the ability to move latex spheres, phage sensitivity, and the ability to digest chitin. gldH encodes a predicted 141-amino-acid protein that localized to the membrane fraction. Labeling studies with [3H]palmitate demonstrated that GldH is a lipoprotein. GldB and GldD, which were previously described, also appear to be lipoproteins. GldH does not exhibit significant amino acid similarity to proteins of known function in the databases. Putative homologs of gldH of unknown function are found in motile (Cytophaga hutchinsonii) and apparently nonmotile (Bacteroides thetaiotaomicron, Bacteroides fragilis, Tannerella forsythensis, Porphyromonas gingivalis, and Prevotella intermedia) members of the Cytophaga-Flavobacterium-Bacteroides group.

scholarly journals Colony spreading of the gliding bacterium Flavobacterium johnsoniae in the absence of the motility adhesin SprB

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Keiko Sato ◽  
Masami Naya ◽  
Yuri Hatano ◽  
Yoshio Kondo ◽  
Mari Sato ◽  
...  
Keyword(s):  
Soft Agar ◽  
Gliding Motility ◽  
Wild Type ◽  
Initial Cell ◽  
Flavobacterium Johnsoniae ◽  
Seeking Behavior ◽  
Colony Spreading ◽  
Gliding Bacterium ◽  
Mutant Cells ◽  
Scanning Electron

AbstractColony spreading of Flavobacterium johnsoniae is shown to include gliding motility using the cell surface adhesin SprB, and is drastically affected by agar and glucose concentrations. Wild-type (WT) and ΔsprB mutant cells formed nonspreading colonies on soft agar, but spreading dendritic colonies on soft agar containing glucose. In the presence of glucose, an initial cell growth-dependent phase was followed by a secondary SprB-independent, gliding motility-dependent phase. The branching pattern of a ΔsprB colony was less complex than the pattern formed by the WT. Mesoscopic and microstructural information was obtained by atmospheric scanning electron microscopy (ASEM) and transmission EM, respectively. In the growth-dependent phase of WT colonies, dendritic tips spread rapidly by the movement of individual cells. In the following SprB-independent phase, leading tips were extended outwards by the movement of dynamic windmill-like rolling centers, and the lipoproteins were expressed more abundantly. Dark spots in WT cells during the growth-dependent spreading phase were not observed in the SprB-independent phase. Various mutations showed that the lipoproteins and the motility machinery were necessary for SprB-independent spreading. Overall, SprB-independent colony spreading is influenced by the lipoproteins, some of which are involved in the gliding machinery, and medium conditions, which together determine the nutrient-seeking behavior.

scholarly journals Flavobacterium johnsoniae GldJ Is a Lipoprotein That Is Required for Gliding Motility

2005 ◽  
Vol 187 (8) ◽  
pp. 2628-2637 ◽  
Author(s):  
Timothy F. Braun ◽  
Mark J. McBride
Keyword(s):  
Protein Expression ◽  
Cell Envelope ◽  
Helical Structure ◽  
Gliding Motility ◽  
Cell Fractionation ◽  
Wild Type ◽  
Unknown Mechanism ◽  
Flavobacterium Johnsoniae

ABSTRACT Cells of Flavobacterium johnsoniae glide rapidly over surfaces by an unknown mechanism. Eight genes required for gliding motility have been described. Complementation of the nonmotile mutant UW102-48 identified another gene, gldJ, that is required for gliding. gldJ mutants formed nonspreading colonies, and individual cells were completely nonmotile. Like previously described nonmotile mutants, gldJ mutants were deficient in chitin utilization and were resistant to bacteriophages that infect wild-type cells. Cell fractionation and labeling studies with [3H]palmitate indicated that GldJ is a lipoprotein. Mutations in gldA, gldB, gldD, gldF, gldG, gldH, or gldI resulted in normal levels of gldJ transcript but decreased levels of GldJ protein. Expression of truncated GldJ protein in wild-type cells resulted in a severe motility defect. GldJ was found in regular bands that suggest the presence of a helical structure within the cell envelope.

scholarly journals Cloning and Characterization of theFlavobacterium johnsoniae Gliding Motility GenesgldD and gldE

2001 ◽  
Vol 183 (14) ◽  
pp. 4167-4175 ◽  
Author(s):  
David W. Hunnicutt ◽  
Mark J. McBride
Keyword(s):  
Membrane Protein ◽  
Cytoplasmic Membrane ◽  
Sequence Similarity ◽  
Gliding Motility ◽  
Wild Type ◽  
Bacteriophage Infection ◽  
Flavobacterium Johnsoniae ◽  
Latex Spheres ◽  
Serovar Typhimurium

ABSTRACT Cells of Flavobacterium johnsoniae move over surfaces by a process known as gliding motility. The mechanism of this form of motility is not known. Cells of F. johnsoniaepropel latex spheres along their surfaces, which is thought to be a manifestation of the motility machinery. Three of the genes that are required for F. johnsoniae gliding motility,gldA, gldB, and ftsX, have recently been described. Tn4351 mutagenesis was used to identify another gene, gldD, that is needed for gliding. Tn4351-induced gldD mutants formed nonspreading colonies, and cells failed to glide. They also lacked the ability to propel latex spheres and were resistant to bacteriophages that infect wild-type cells. Introduction of wild-type gldD into the mutants restored motility, ability to propel latex spheres, and sensitivity to bacteriophage infection. gldD codes for a cytoplasmic membrane protein that does not exhibit strong sequence similarity to proteins of known function. gldE, which lies immediately upstream ofgldD, encodes another cytoplasmic membrane protein that may be involved in gliding motility. Overexpression ofgldE partially suppressed the motility defects of agldB point mutant, suggesting that GldB and GldE may interact. GldE exhibits sequence similarity to Borrelia burgdorferi TlyC and Salmonella enterica serovar Typhimurium CorC.

scholarly journals Flavobacterium johnsoniae Gliding Motility Genes Identified by mariner Mutagenesis

2005 ◽  
Vol 187 (20) ◽  
pp. 6943-6952 ◽  
Author(s):  
Timothy F. Braun ◽  
Manjeet K. Khubbar ◽  
Daad A. Saffarini ◽  
Mark J. McBride
Keyword(s):  
Complete Loss ◽  
Gliding Motility ◽  
Wild Type ◽  
Flavobacterium Johnsoniae ◽  
Chemically Induced

ABSTRACT Cells of Flavobacterium johnsoniae glide rapidly over surfaces. The mechanism of F. johnsoniae gliding motility is not known. Eight gld genes required for gliding motility have been described. Disruption of any of these genes results in complete loss of gliding motility, deficiency in chitin utilization, and resistance to bacteriophages that infect wild-type cells. Two modified mariner transposons, HimarEm1 and HimarEm2, were constructed to allow the identification of additional motility genes. HimarEm1 and HimarEm2 each transposed in F. johnsoniae, and nonmotile mutants were identified and analyzed. Four novel motility genes, gldK, gldL, gldM, and gldN, were identified. GldK is similar in sequence to the lipoprotein GldJ, which is required for gliding. GldL, GldM, and GldN are not similar in sequence to proteins of known function. Cells with mutations in gldK, gldL, gldM, and gldN were defective in motility and chitin utilization and were resistant to bacteriophages that infect wild-type cells. Introduction of gldA, gldB, gldD, gldFG, gldH, gldI, and gldJ and the region spanning gldK, gldL, gldM, and gldN individually into 50 spontaneous and chemically induced nonmotile mutants restored motility to each of them, suggesting that few additional F. johnsoniae gld genes remain to be identified.

scholarly journals Flavobacterium johnsoniae gldN and gldO Are Partially Redundant Genes Required for Gliding Motility and Surface Localization of SprB

2009 ◽  
Vol 192 (5) ◽  
pp. 1201-1211 ◽  
Author(s):  
Ryan G. Rhodes ◽  
Mudiarasan Napoleon Samarasam ◽  
Abhishek Shrivastava ◽  
Jessica M. van Baaren ◽  
Soumya Pochiraju ◽  
...  
Keyword(s):  
Protein Secretion ◽  
Deletion Mutant ◽  
Gliding Motility ◽  
Selection Strategy ◽  
Wild Type ◽  
Flavobacterium Johnsoniae ◽  
Redundant Genes ◽  
Surface Localization ◽  
Gliding Bacterium ◽  
Mutant Cells

ABSTRACT Cells of the gliding bacterium Flavobacterium johnsoniae move rapidly over surfaces. Mutations in gldN cause a partial defect in gliding. A novel bacteriophage selection strategy was used to aid construction of a strain with a deletion spanning gldN and the closely related gene gldO in an otherwise wild-type F. johnsoniae UW101 background. Bacteriophage transduction was used to move a gldN mutation into F. johnsoniae UW101 to allow phenotypic comparison with the gldNO deletion mutant. Cells of the gldN mutant formed nonspreading colonies on agar but retained some ability to glide in wet mounts. In contrast, cells of the gldNO deletion mutant were completely nonmotile, indicating that cells require GldN, or the GldN-like protein GldO, to glide. Recent results suggest that Porphyromonas gingivalis PorN, which is similar in sequence to GldN, has a role in protein secretion across the outer membrane. Cells of the F. johnsoniae gldNO deletion mutant were defective in localization of the motility protein SprB to the cell surface, suggesting that GldN may be involved in secretion of components of the motility machinery. Cells of the gldNO deletion mutant were also deficient in chitin utilization and were resistant to infection by bacteriophages, phenotypes that may also be related to defects in protein secretion.

scholarly journals SprB Is a Cell Surface Component of the Flavobacterium johnsoniae Gliding Motility Machinery

2008 ◽  
Vol 190 (8) ◽  
pp. 2851-2857 ◽  
Author(s):  
Shawn S. Nelson ◽  
Sreelekha Bollampalli ◽  
Mark J. McBride
Keyword(s):  
Cell Surface ◽  
Surface Protein ◽  
Gliding Motility ◽  
Wild Type ◽  
Polystyrene Microspheres ◽  
Flavobacterium Johnsoniae ◽  
A Cell ◽  
Transposon Insertions ◽  
Gliding Bacterium ◽  
Surface Adhesins

ABSTRACT Cells of the gliding bacterium Flavobacterium johnsoniae move rapidly over surfaces by an unknown mechanism. Transposon insertions in sprB resulted in cells that were defective in gliding. SprB is a highly repetitive 669-kDa cell surface protein, and antibodies against SprB inhibited the motility of wild-type cells. Polystyrene microspheres coated with antibodies against SprB attached to and were rapidly propelled along the cell surface, suggesting that SprB is one of the outermost components of the motility machinery. The movement of SprB along the cell surface supports a model of gliding motility in which motors anchored to the cell wall rapidly propel cell surface adhesins.

scholarly journals Role of rpoS in Stress Survival and Virulence of Vibrio cholerae

1998 ◽  
Vol 180 (4) ◽  
pp. 773-784 ◽  
Author(s):  
Fitnat H. Yildiz ◽  
Gary K. Schoolnik
Keyword(s):  
Vibrio Cholerae ◽  
Genomic Library ◽  
Bacterial Species ◽  
Wild Type ◽  
Reading Frame ◽  
Infant Mouse ◽  
Acid Protein ◽  
Amino Acid Protein

ABSTRACT Vibrio cholerae is known to persist in aquatic environments under nutrient-limiting conditions. To analyze the possible involvement of the alternative sigma factor encoded byrpoS, which is shown to be important for survival during nutrient deprivation in several other bacterial species, a V. cholerae rpoS homolog was cloned by functional complementation of an Escherichia coli mutant by using a wild-type genomic library. Sequence analysis of the complementing clone revealed an 1.008-bp open reading frame which is predicted to encode a 336-amino-acid protein with 71 to 63% overall identity to other reported rpoS gene products. To determine the functional role of rpoS in V. cholerae, we inactivatedrpoS by homologous recombination. V. choleraestrains lacking rpoS are impaired in the ability to survive diverse environmental stresses, including exposure to hydrogen peroxide, hyperosmolarity, and carbon starvation. These results suggest that rpoS may be required for the persistence of V. cholerae in aquatic habitats. In addition, the rpoSmutation led to reduced production or secretion of hemagglutinin/protease. However, rpoS is not critical for in vivo survival, as determined by an infant mouse intestinal competition assay.

scholarly journals Chrysanthemum DgWRKY2 Gene Enhances Tolerance to Salt Stress in Transgenic Chrysanthemum

2018 ◽  
Vol 19 (7) ◽  
pp. 2062 ◽  
Author(s):  
Ling He ◽  
Yin-Huan Wu ◽  
Qian Zhao ◽  
Bei Wang ◽  
Qing-Lin Liu ◽  
...  
Keyword(s):  
Salt Stress ◽  
Sugar Content ◽  
Soluble Sugar ◽  
Wild Type ◽  
Acid Protein ◽  
Transgenic Lines ◽  
High Salt Stress ◽  
Transgenic Chrysanthemum ◽  
Stress Related Genes ◽  
Amino Acid Protein

WRKY transcription factors (TFs) play a vital part in coping with different stresses. In this study, DgWRKY2 was isolated from Dendranthema grandiflorum. The gene encodes a 325 amino acid protein, belonging to the group II WRKY family, and contains one typical WRKY domain (WRKYGQK) and a zinc finger motif (C-X4-5-C-X22-23-H-X1-H). Overexpression of DgWRKY2 in chrysanthemum enhanced tolerance to high-salt stress compared to the wild type (WT). In addition, the activities of antioxidant enzymes (superoxide dismutase (SOD), peroxidase (POD), catalase (CAT)), proline content, soluble sugar content, soluble protein content, and chlorophyll content of transgenic chrysanthemum, as well as the survival rate of the transgenic lines, were on average higher than that of the WT. On the contrary, hydrogen peroxide (H2O2), superoxide anion (O2−), and malondialdehyde (MDA) accumulation decreased compared to WT. Expression of the stress-related genes DgCAT, DgAPX, DgZnSOD, DgP5CS, DgDREB1A, and DgDREB2A was increased in the DgWRKY2 transgenic chrysanthemum compared with their expression in the WT. In conclusion, our results indicate that DgWRKY2 confers salt tolerance to transgenic chrysanthemum by enhancing antioxidant and osmotic adjustment. Therefore, this study suggests that DgWRKY2 could be used as a reserve gene for salt-tolerant plant breeding.

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