Cryo‐electron tomography analyses of terminal organelle mutants suggest the motility mechanism of <i>Mycoplasma genitalium</i>

Seybert, Anja; González-González, Luis; Scheffer, Margot P.; Lluch‐Senar, María; Mariscal, Ana M.; Querol, Enrique; Matthaeus, Franziska; Piñol, Jaume; Frangakis, Achilleas S.

doi:10.1111/mmi.13938

Cited by 19 publications

(21 citation statements)

References 38 publications

(63 reference statements)

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“…M. pneumoniae -type gliding has until now been studied mainly in M. pneumoniae and Mycoplasma genitalium . A structure outline of the gliding machinery has been suggested, including that for fifteen component proteins (6-8, 11). The gliding machinery, called the ‘attachment organelle,’ is composed of an internal core and adhesin complexes (12-14).…”

Section: Introductionmentioning

confidence: 99%

Behaviors and Energy Source ofMycoplasma gallisepticumGliding

Mizutani

Miyata

2019

Preprint

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Mycoplasma gallisepticum, an avian-pathogenic bacterium, glides on host tissue surfaces by using a common motility system with Mycoplasma pneumoniae. In the present study, we observed and analyzed the gliding behaviors of M. gallisepticum in detail by using optical microscopes. M. gallisepticum glided at a speed of 0.27 ± 0.09 µm/s with directional changes relative to the cell axis of 0.6 ± 44.6 degrees/5 s without the rolling of the cell body. To examine the effects of viscosity on gliding, we analyzed the gliding behaviors under viscous environments. The gliding speed was constant in various concentrations of methylcellulose but was affected by Ficoll. To investigate the relationship between binding and gliding, we analyzed the inhibitory effects of sialyllactose on binding and gliding. The binding and gliding speed sigmoidally decreased with sialyllactose concentration, indicating the cooperative binding of the cell. To determine the direct energy source of gliding, we used a membrane-permeabilized ghost model. We permeabilized M. gallisepticum cells with Triton X-100 or Triton X-100 containing ATP and analyzed the gliding of permeabilized cells. The cells permeabilized with Triton X-100 did not show gliding; in contrast, the cells permeabilized with Triton X-100 containing ATP showed gliding at a speed of 0.014 ± 0.007 μm/s. These results indicate that the direct energy source for the gliding motility of M. gallisepticum is ATP.IMPORTANCEMycoplasmas, the smallest bacteria, are parasitic and occasionally commensal. Mycoplasma gallisepticum is related to human pathogenic Mycoplasmas—Mycoplasma pneumoniae and Mycoplasma genitalium—which causes so-called ‘walking pneumonia’ and non-gonococcal urethritis, respectively. These Mycoplasmas trap sialylated oligosaccharides, which are common targets among influenza viruses, on host trachea or urinary tract surfaces and glide to enlarge the infected areas. Interestingly, this gliding motility is not related to other bacterial motilities or eukaryotic motilities. Here, we quantitatively analyze cell behaviors in gliding and clarify the direct energy source. The results provide clues for elucidating this unique motility mechanism.

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Section: Introductionmentioning

confidence: 99%

Behaviors and Energy Source ofMycoplasma gallisepticumGliding

Mizutani

Miyata

2019

Preprint

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“…M. pneumoniae-type gliding has until now been studied mainly in M. pneumoniae and Mycoplasma genitalium. A structure outline of the gliding machinery has been suggested, including that for 15 component proteins (6)(7)(8)11). The gliding machinery, called the "attachment organelle," is composed of an internal core and adhesin complexes (12)(13)(14).…”

mentioning

confidence: 99%

Behaviors and Energy Source of Mycoplasma gallisepticum Gliding

Mizutani

Miyata

2019

J Bacteriol

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Mycoplasma gallisepticum, an avian-pathogenic bacterium, glides on host tissue surfaces by using a common motility system with Mycoplasma pneumoniae. In the present study, we observed and analyzed the gliding behaviors of M. gallisepticum in detail by using optical microscopes. M. gallisepticum glided at a speed of 0.27 ± 0.09 μm/s with directional changes relative to the cell axis of 0.6 degree ± 44.6 degrees/5 s without the rolling of the cell body. To examine the effects of viscosity on gliding, we analyzed the gliding behaviors under viscous environments. The gliding speed was constant in various concentrations of methylcellulose but was affected by Ficoll. To investigate the relationship between binding and gliding, we analyzed the inhibitory effects of sialyllactose on binding and gliding. The binding and gliding speed sigmoidally decreased with sialyllactose concentration, indicating the cooperative binding of the cell. To determine the direct energy source of gliding, we used a membrane-permeabilized ghost model. We permeabilized M. gallisepticum cells with Triton X-100 or Triton X-100 containing ATP and analyzed the gliding of permeabilized cells. The cells permeabilized with Triton X-100 did not show gliding; in contrast, the cells permeabilized with Triton X-100 containing ATP showed gliding at a speed of 0.014 ± 0.007 μm/s. These results indicate that the direct energy source for the gliding motility of M. gallisepticum is ATP. IMPORTANCE Mycoplasmas, the smallest bacteria, are parasitic and occasionally commensal. Mycoplasma gallisepticum is related to human-pathogenic mycoplasmas—Mycoplasma pneumoniae and Mycoplasma genitalium—which cause so-called “walking pneumonia” and nongonococcal urethritis, respectively. These mycoplasmas trap sialylated oligosaccharides, which are common targets among inﬂuenza viruses, on host trachea or urinary tract surfaces and glide to enlarge the infected areas. Interestingly, this gliding motility is not related to other bacterial motilities or eukaryotic motilities. Here, we quantitatively analyze cell behaviors in gliding and clarify the direct energy source. The results provide clues for elucidating this unique motility mechanism.

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“…The main virulence factor in the pathogenesis of the species of Mycoplasma is the ability of these organisms to adhere to the host's epithelial mucus membrane and colonize the affected tissue [6]. Many mycoplasmas rely on the concentration of adhesins and adhesin-related accessory proteins at the cytadherence tip organelle ( Figure 2) for attachment and motility [38][39][40]. None of the genes encoding the adhesins and adhesin-related accessory proteins have homologs across the various species and are not part of the core genome of these organisms.…”

Section: Virulence Factors In Hostmycoplasma Attachmentmentioning

confidence: 99%

Virulence and molecular adaptation of human urogenital mycoplasmas: a review

Roachford

Nelson

Mohapatra

2019

Biotechnology & Biotechnological Equipment

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The pathogenesis of mycoplasmas requires their attachment to the epithelial mucosa membrane of the host cells, followed by colonisation and necrotic destruction of the submucosal tissue. The extent of this pathogenesis depends on the ability of species of Mycoplasma to effectively attach and invade the host's tissue. In this regard, the cytadherence tip organelle has evolved within the mycoplasmas to accomplish this feat. However, species of Mycoplasma that do not possess the specialized structure remain virulent with the use of surface-membrane lipoproteins. The lipoprotein ligands bind to sulfatides and sialoglycoconjugates on the host's mucosa membranes. This hostmycoplasma interaction, though poorly studied, appears to have a wide underlying array of complex molecular mechanisms, which after activation trigger cytadherence, immunomodulation and virulence. Mycoplasmas with their highly redundant minimal genomes display dynamic genotypic and phenotypic plasticity; a trait that has allowed them to adapt, persist and survive successfully in adverse niches through circumvention and tempering of the host's humoral immune response. Additionally, the linkages between the mycoplasmas persistence and chronic inflammatory diseases in humans necessitate examining the host-mycoplasma interaction at the proteogenomic level. This paper provides an overview on the molecular mechanisms involved in cytadherence, surfacemembrane antigenic variation and survival strategies of human urogenital mycoplasmas.

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Cryo‐electron tomography analyses of terminal organelle mutants suggest the motility mechanism of Mycoplasma genitalium

Cited by 19 publications

References 38 publications

Behaviors and Energy Source ofMycoplasma gallisepticumGliding

Behaviors and Energy Source ofMycoplasma gallisepticumGliding

Behaviors and Energy Source of Mycoplasma gallisepticum Gliding

Virulence and molecular adaptation of human urogenital mycoplasmas: a review

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