SEARCH · PubMed Health

Results for “twitching motility”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

PubMed1980

A function of Pseudomonas aeruginosa PAO polar pili: twitching motility.

Twitching motility is a mode of flagella-independent surface translocation exhibited by Pseudomonas aeruginosa and other bacteria on solid media. All species exhibiting it carry thin pili, usually polar. This work shows that only PAO and K strains of P. aeruginosa with retractile (PSA) pili were able to move in this way, those with no pili or non-retractile pili remaining stationary. Specific agents such as anti-pilus serum, which prevents otherwise functional pili from retracting, also prevented twitching motility.

Fimbriae, Bacterial↗

PubMed2000

Pilus retraction powers bacterial twitching motility.

Twitching and social gliding motility allow many gram negative bacteria to crawl along surfaces, and are implicated in a wide range of biological functions. Type IV pili (Tfp) are required for twitching and social gliding, but the mechanism by which these filaments promote motility has remained enigmatic. Here we use laser tweezers to show that Tfp forcefully retract. Neisseria gonorrhoeae cells that produce Tfp actively crawl on a glass surface and form adherent microcolonies. When laser tweezers are used to place and hold cells near a microcolony, retractile forces pull the cells toward the microcolony. In quantitative experiments, the Tfp of immobilized bacteria bind to latex beads and retract, pulling beads from the tweezers at forces that can exceed 80 pN. Episodes of retraction terminate with release or breakage of the Tfp tether. Both motility and retraction mediated by Tfp occur at about 1 microm s(-1) and require protein synthesis and function of the PilT protein. Our experiments establish that Tfp filaments retract, generate substantial force and directly mediate cell movement.

Fimbriae, Bacterial↗

PubMed1999

A re-examination of twitching motility in Pseudomonas aeruginosa.

Twitching motility is a form of solid surface translocation which occurs in a wide range of bacteria and which is dependent on the presence of functional type IV fimbriae or pili. A detailed examination of twitching motility in Pseudomonas aeruginosa under optimal conditions in vitro was carried out. Under these conditions (at the smooth surface formed between semi-solid growth media and plastic or glass surfaces) twitching motility is extremely rapid, leading to an overall radial rate of colony expansion of 0.6 mm h(-1) or greater. The zones of colony expansion due to twitching motility are very thin and are best visualized by staining. These zones exhibit concentric rings in which there is a high density of microcolonies, which may reflect periods of expansion and consolidation/cell division. Video microscopic analysis showed that twitching motility involves the initial formation of large projections or rafts of aggregated cells which move away from the colony edge. Behind the rafts, individual cells move rapidly up and down trails which thin and branch out, ultimately forming a fine lattice-like network of cells. The bacteria in the lattice network then appear to settle and divide to fill out the colonized space. Our observations redefine twitching motility as a rapid, highly organized mechanism of bacterial translocation by which P. aeruginosa can disperse itself over large areas to colonize new territories. It is also now clear, both morphologically and genetically, that twitching motility and social gliding motility, such as occurs in Myxococcus xanthus, are essentially the same process.

Fimbriae, Bacterial↗

PubMed2001

Twitching motility of Ralstonia solanacearum requires a type IV pilus system.

Twitching motility is a form of bacterial translocation over firm surfaces that requires retractile type IV pili. Microscopic colonies of Ralstonia solanacearum strains AW1, K60 and GMI1000 growing on the surface of a rich medium solidified with 1.6% agar appeared to exhibit twitching motility, because early on they divided into motile 'rafts' of cells and later developed protruding 'spearheads' at their margins. Individual motile bacteria were observed only when they were embedded within masses of other cells. Varying degrees of motility were observed for 33 of 35 strains of R. solanacearum in a selected, diverse collection. Timing was more important than culture conditions for observing motility, because by the time wild-type colonies were easily visible by eye (about 48 h) this activity ceased and the spearheads were obscured by continued bacterial multiplication. In contrast, inactivation of PhcA, a transcriptional regulator that is essential for R. solanacearum to cause plant disease, resulted in colonies that continued to expand for at least several additional days. Multiple strains with mutations in regulatory genes important for virulence were tested, but all exhibited wild-type motility. Many of the genes required for production of functional type IV pili, and hence for twitching motility, are conserved among unrelated bacteria, and pilD, pilQ and pilT orthologues were identified in R. solanacearum. Colonies of R. solanacearum pilQ and pilT mutants did not develop spearheads or rafts, confirming that the movement of cells that had been observed was due to twitching motility. Compared to the wild-type parents, both pilQ and pilT mutants caused slower and less severe wilting on susceptible tomato plants. This is the first report of twitching motility by a phytopathogenic bacterium, and the first example where type IV pili appear to contribute significantly to plant pathogenesis.

Adenosine Triphosphatases↗

PubMed1999

Roles of Pseudomonas aeruginosa las and rhl quorum-sensing systems in control of twitching motility.

Pseudomonas aeruginosa is a ubiquitous environmental bacterium and an important human pathogen. The production of several virulence factors by P. aeruginosa is controlled through two quorum-sensing systems, las and rhl. We have obtained evidence that both the las and rhl quorum-sensing systems are also required for type 4 pilus-dependent twitching motility and infection by the pilus-specific phage D3112cts. Mutants which lack the ability to synthesize PAI-1, PAI-2, or both autoinducers were significantly or greatly impaired in twitching motility and in susceptibility to D3112cts. Twitching motility and phage susceptibility in the autoinducer-deficient mutants were partially restored by exposure to exogenous PAI-1 and PAI-2. Both twitching motility and infection by pilus-specific phage are believed to be dependent on the extension and retraction of polar type 4 pili. Western blot analysis of whole-cell lysates and enzyme-linked immunosorbent assays of intact cells were used to measure the amounts of pilin on the cell surfaces of las and rhl mutants relative to that of the wild type. It appears that PAI-2 plays a crucial role in twitching motility and phage infection by affecting the export and assembly of surface type 4 pili. The ability of P. aeruginosa cells to adhere to human bronchial epithelial cells was also found to be dependent on the rhl quorum-sensing system. Microscopic analysis of twitching motility indicated that mutants which were unable to synthesize PAI-1 were defective in the maintenance of cellular monolayers and migrating packs of cells. Thus, PAI-1 appears to have an essential role in maintaining cell-cell spacing and associations required for effective twitching motility.

Bacterial Adhesion↗

PubMed1994

Characterization of a gene, pilU, required for twitching motility but not phage sensitivity in Pseudomonas aeruginosa.

Type 4 fimbriae (or pilli) are associated with a form of bacterial surface translocation known as twitching motility. Fimbriae are also associated with sensitivity to certain bacteriophages such as PO4. Transposon mutagenesis was used to generate a library of Pseudomonas aeruginosa mutants which lack the spreading-colony morphology characteristic of twitching motility. In four of these mutants the transposon was found to be located in the vicinity of the previously described pilT locus, but in only one case was it found to have inserted within the pilT coding sequence. Two twitching-motility mutants originally isolated by Bradley, K2.2, and PAO2001.2, which have been widely used in studies of P. aeruginosa fimbrial structure and expression, were also shown to affect pilT and to comprise a small deletion and a frameshift mutation, respectively. The other three transposon mutations were found to have occurred within a new gene located directly downstream of pilT. This gene, termed pilU, encodes a 382-amino-acid protein closely related to PilT and to other members of a family of putative nucleotide-binding proteins which are involved in the assembly of cell surface-associated complexes. Furthermore, the pilT and pilU genes appear to be independently expressed. Like pilT mutants, the pilU mutants were hyperfimbriate, but in neither case was this associated with an increase in transcription of the fimbrial subunit gene pilA. However, in contrast to pilT mutants, the pilU mutants had not also acquired resistance to infection by bacteriophage PO4. A broader survey showed differential patterns of sensitivity to various fimbrial-specific phages among the pilU mutants and other twitching-motility mutants in the transposon library. The fact that twitching motility is not obligatorily associated with phage sensitivity suggests that the latter may not be directly dependent upon fimbrial function but rather may be a consequence of some common factor(s) involved in their assembly or export pathways.

Adenosine Triphosphatases↗

PubMed2000

Identification of a novel gene, fimV, involved in twitching motility in Pseudomonas aeruginosa.

Transposon mutagenesis was used to identify a new locus required for twitching motility in Pseudomonas aeruginosa. Four Tn5-B21 mutants which lacked twitching motility and a fifth which exhibited impaired motility were found to map to the same KPN:I restriction fragment at approximately 40 min on the P. aeruginosa genome. Cloning and sequencing studies showed that all five transposon insertions occurred within the same 2.8 kb ORF, which was termed fimV. The product of this gene has a putative peptidoglycan-binding domain, predicted transmembrane domains, a highly acidic C terminus and anomalous electrophoretic migration, indicating unusual primary or secondary structure. The P. aeruginosa genome also possesses a paralogue of fimV. Homologues of fimV were also found in the sequenced genomes of the other type-IV-fimbriated bacteria Neisseria gonorrhoeae, Neisseria meningitidis, Legionella pneumophila and Vibrio cholerae, but not in those of other bacteria which lack type IV fimbriae. A fimV homologue was also found in the genome sequence of Shewanella putrefaciens, along with many other homologues of type IV fimbrial genes, indicating that this bacterium is also likely to produce type IV fimbriae. Wild-type twitching motility was restored to fimV mutants by complementation in a dosage-dependent manner. Overexpression of fimV resulted in an unusual phenotype where the cells were massively elongated and migrated in large convoys at the periphery of the colony. It is suggested that FimV may be involved in remodelling of the peptidoglycan layer to enable assembly of the type IV fimbrial structure and machinery.

Animals↗

PubMed1991

Characterisation of a Pseudomonas aeruginosa twitching motility gene and evidence for a specialised protein export system widespread in eubacteria.

Type-4 fimbriae (pili) are associated with a phenomenon known as twitching motility, which appears to be involved with bacterial translocation across solid surfaces. Pseudomonas aeruginosa mutants which produce fimbriae, but which have lost the twitching motility function, display altered colony morphology and resistance to fimbrial-specific bacteriophage. We have used phenotypic complementation of such mutants to isolate a region of DNA involved in twitching motility. This region was physically mapped to a SpeI fragment around 20 min on the P. aeruginosa PAO chromosome, remote from the major fimbrial locus (around 75 min) where the structural subunit-encoding gene (fimA/pilA) and ancillary genes required for fimbrial assembly (pilB, C and D) are found. A gene, pilT, within the twitching motility region is predicted to encode a 344-amino acid protein which has strong homology to a variety of other bacterial proteins. These include the P. aeruginosa PilB protein, the ComG ORF-1 protein from the Bacillus subtilis comG operon (necessary for competence), the PulE protein from the Klebsiella oxytoca (formerly K. pneumoniae) pulC-O operon (involved in pullulanase export), and the VirB-11 protein from the virB operon (involved in virulence) which is located on the Agrobacterium tumefaciens Ti plasmid. We have also identified other sets of homologies between P. aeruginosa fimbrial assembly (Pil) proteins and B. subtilis Com and K. oxytoca Pul proteins, which suggest that these are all related members of a specialised protein export pathway which is widespread in the eubacteria.

Amino Acid Sequence↗

PubMed1975

The influence of changes in the environment on twitching motility.

By examining medium composition and cultural conditions quantitatively it was possible to define conditions suitable to bring twitching motility about. Such conditions include the use of freshly poured, relatively thick and only slightly dried plates of a dilute medium in which the agar concentration is not too high. Incubation should take place in a humid atmosphere. In fact, everything points to the humidity as a factor of the utmost importance. Using strains of Acinetobacter calcoaceticus, it was found that a pH value of the medium adjusted to 9.0 enhances twitching motility. Spreading growth was not produced if agarose was applied instead of ordinary agars. Twitching motility was inhibited by a number of different chlorides, potassium nitrate, Tween 80 and sodium taurocholate. Possible interpretations of these observations are discussed.

Acinetobacter↗

PubMed1975

On twitching motility and its mechanism.

Previously published reports have established a correlation between twitching motility and the possession of polar fimbriae in all cases examined. Twitching motility was shown to be highly dependent on the availability of liquid at the agar surface. In the present paper experiments are reported that establish: 1) the dependence of twitching on the existence of a layer of liquid of a particular thickness, 2) the production of such a liquid layer surrounding areas of growing organisms, and 3) the affinity of twitching bacteria for the air-water interface. Reasoning from these facts, it is postulated that the demonstrated affinity for the air-water interface is conferred upon the cells by the polar fimbriae. It is also suggested how the movements might be generated.

Bacterial Physiological Phenomena↗

PubMed1975

Correlation between twitching motility and possession of polar fimbriae in Acinetobacter calcoaceticus.

Negatively stained preparations of 16 strains of Acinetobacter calcoaceticus were examined in the electron microscope. Five of the strains did and 11 of the strains did not exhibit twitching motility. Two of the non-twitching strains were substrains of twitching wild-type strains. All twitching strains were found to possess fimbriae with a diameter of approximately 50 A. These fimbriae were shown to be of polar origin except in one strain where, for technical reasons, the origin could not be determined with certainty. Polar fimbriae could not be demonstrated in any of the strains that did not exhibit twitching motility. The demonstration of polar fimbriae was only regularly possible during the exponential growth phase, presumably because the fimbriae are shed by the bacteria during later growth phases. During the study, methods were developed for securing exponentially growing bacteria in concentrations suited for the preparation of negatively stained cells for electron microscopy. Peritrichously arranged fimbriae with a diameter of approximately 30 A were demonstrated in nearly all strains studied, especially on cells in late growth phases. The occurrence of this kind of fimbriae was therefore not correlated with the occurrence of twitching motility.

Acinetobacter↗

PubMed1994

Characterization of a Pseudomonas aeruginosa gene cluster involved in pilus biosynthesis and twitching motility: sequence similarity to the chemotaxis proteins of enterics and the gliding bacterium Myxococcus xanthus.

The type 4 pili of Pseudomonas aeruginosa are important cell-associated virulence factors that play a crucial role in mediating (i) bacterial adherence to, and colonization of, mucosal surfaces, (ii) a novel mode of flagella-independent surface translocation known as 'twitching motility', and (iii) the initial stages of the infection process for a number of bacteriophages. A new set of loci involved in pilus biogenesis and twitching motility was identified based on the ability of DNA sequences downstream of the pilG gene to complement the non-piliated (pil) strain, PAO6609. Sequence analysis of a 3.2 kb region directly downstream of pilG revealed the presence of three genes, which have been designated pilH, pilI, and pilJ. The predicted translation product of the pilH gene (13,272 Da), like PilG, exhibits significant amino acid identity with the enteric single-domain response regulator CheY. The putative PilI protein (19,933 Da) is 28% identical to the FrzA protein, a CheW homologue of the gliding bacterium Myxococcus xanthus, and the PilJ protein (72,523 Da) is 26% identical to the enteric methyl-accepting chemotaxis protein (MCP) Tsr. Mutants containing insertions in pilI and pilJ were severely impaired in their ability to produce pili and did not translocate across solid surfaces. The pilH mutant remained capable of pilus production and twitching motility, but displayed an altered motility pattern characterized by the presence of many doughnut-shaped swirls. Each of these pil mutants, however, produced zones that were at least as large as the parent in flagellar-mediated swarm assays. The sequence similarities between the putative pilG, H, I and J gene products and several established chemotaxis proteins, therefore, lend strong support to the hypothesis that these proteins are part of a signal-transduction network that controls P. aeruginosa pilus biosynthesis and twitching motility.

Amino Acid Sequence↗

PubMed1975

The occurrence of twitching motility among gram-negative bacteria.

Almost 1000 strains representing well above 50 different species or groups of gram-negative bacteria were examined for twitching motility. This kind of motility was mainly found in strictly aerobic cocci and rods (viz. Acinetobacter calcoaceticus, Moraxella spp., Neisseria gonorrhoeae, N. meningitidis, Pseudomonas spp., phenon 3 of Thornley that is closely related to Acinetobacter, and marine, yellow-pigmented rods), but also in the facultative Eikenella corrodens and in anaerobic strains presumptively identified as "Bacteroides corrodens" earlier. Strains of species known to possess polar fimbriae were shown to exhibit twitching motility. None of the strains of species known to possess peritrichously arranged fimbriae exhibited twitching motility.

Acinetobacter↗

PubMed1996

The alginate regulator AlgR and an associated sensor FimS are required for twitching motility in Pseudomonas aeruginosa.

Mucoid strains of Pseudomonas aeruginosa isolated from the lungs of cystic fibrosis patients produce large amounts of the exopolysaccharide alginate. AlgR has long been considered a key regulator of alginate production, but its cognate sensor has not been identified. Here we show that AlgR is required for twitching motility, which is a form of bacterial surface translocation mediated by type 4 fimbriae. Adjacent to algR we have identified a sensor gene (fimS), which is also required for twitching motility. However, FimS does not appear to be required for alginate production in mucoid strains. FimS and AlgR are representative of a new subclass of two-component transmitter-receiver regulatory systems. The alternative sigma factor AlgU also affects both alginate production and twitching motility. Therefore, these two virulence determinants appear to be closely associated and coordinately regulated.

Alginates↗

PubMed1998

PilT mutations lead to simultaneous defects in competence for natural transformation and twitching motility in piliated Neisseria gonorrhoeae.

Neisseria gonorrhoeae, the Gram-negative aetiological agent of gonorrhoeae, is one of many mucosal pathogens of man that expresses competence for natural transformation. Expression of this phenotype by gonococci appears to rely on the expression of type IV pili (Tfp), but the mechanistic basis for this relationship remains unknown. During studies of gonococcal pilus biogenesis, a homologue of the PilT family of proteins, required for Tfp-dependent twitching motility in Pseudomonas aeruginosa and social gliding motility in Myxococcus xanthus, was discovered. Like the findings in these other species, we show here that gonococcal PilT mutants constructed in vitro no longer display twitching motility. In addition, we demonstrate that they have concurrently lost the ability to undergo natural transformation, despite the expression of structurally and morphologically normal Tpf. These results were confirmed by the findings that two classes of spontaneous mutants that failed to express twitching motility and transformability carried mutations in PilT. Piliated PilT mutants and a panel of pilus assembly mutants were found to be deficient in sequence-specific DNA uptake into the cell, the earliest demonstrable step in neisserial competence. The PilT-deficient strains represent the first genetically defined mutants that are defective in DNA uptake but retain Tfp expression.

Adenosine Triphosphatases↗

PubMed2001

Pseudomonas aeruginosa exhibits directed twitching motility up phosphatidylethanolamine gradients.

Pseudomonas aeruginosa translocates over solid surfaces by a type IV pilus-dependent form of multicellular motility known as twitching. We wondered whether cells utilize endogenous factors to organize twitching, and we purified from wild-type cells a lipid that caused directed movement. Wild-type P. aeruginosa, but not a pilJ pilus-deficient mutant, showed biased movement up gradients of phosphatidylethanolamine (PE) established in agar. Activity was related to the fatty acid composition of the lipid, as two synthetic PE species, dilauroyl and dioleoyl PE, were capable of directing P. aeruginosa motility while many other species were inactive. P. aeruginosa PE did not contain either laurate or oleate, implying that the native attractant species contains different fatty acids. Uniform concentrations of PE increased cell velocity, suggesting that chemokinesis may be at least partly responsible for directed movement. We speculate that PE-directed twitching motility may be involved in biofilm formation and pathogenesis.

Chemotactic Factors↗

PubMed1997

Molecular genetic analysis of type-4 pilus biogenesis and twitching motility using Pseudomonas aeruginosa as a model system--a review.

Genetic analysis of Pseudomonas aeruginosa pilus biogenesis and twitching motility has revealed the requirement for several pil loci which have been localized to different regions of the chromosome. One pil locus, designated pilE, resides at approx. 71 min on the PAO genetic map, a region of the chromosome previously shown to harbor a number of genes required for pilus assembly (i.e., pilA, -B, -C, -D, -R and -S). The PilE protein shows significant sequence identity to the N-terminal domain of PilA as well as to the pilin precursors from a variety of type-4 pilus producers. Included within this homologous region is a short, positively charged leader sequence followed by a prepilin peptidase cleavage site and a largely hydrophobic region. Additionally, an unlinked set of pil genes, designated pilG, -H, -I, -J and -K, has been localized to the SpeI fragment H which corresponds to approx. 20 min on the PAO genetic map. This gene cluster encodes proteins that demonstrate remarkable similarity to the chemotaxis proteins of enterics and the gliding bacterium Myxococcus xanthus and are thought to be part of a signal transduction system that controls P. aeruginosa pilus biosynthesis and twitching motility.

Bacterial Outer Membrane Proteins↗

PubMed1975

Twitching motility and possession of polar fimbriae in spreading Streptococcus sanguis isolates from the human throat.

A collection of 19 strains of alpha haemolytic streptococci, isolated from throat swabs and characterized by production of spreading zones around colonies on blood agar, was found to constitute a very homogeneous group with morphological, physiological and biochemical characters corresponding to those of streptococci of ser-group H, or Streptococcus sanguis, and they all appeared to possess the group H antigen. They all had a common agglutinogen and, in addition, heterogeneous agglutinogens. The spreading growth, which appears to be a common property of S. sanguis, was due to twitching motility, and the spreading cultures possessed polar fimbriae. tneither twitching motility nor the possession of polar fimbriae have been observed in gram-positive bacteria before.

Agglutination Tests↗