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Behaviors and Energy Source of Mycoplasma gallisepticum Gliding
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ABSTRACT
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.
IMPORTANCE
Mycoplasmas
, 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.
Title: Behaviors and Energy Source of
Mycoplasma gallisepticum
Gliding
Description:
ABSTRACT
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.
IMPORTANCE
Mycoplasmas
, 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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