Researchers have identified how the
pathogenic bacterium Pseudomonas
aeruginosa uses tension-activated membrane channels to stop itself from
swelling up and bursting when it is suddenly exposed to water. The study helps
explain how this bacterium -- a major cause of hospital-acquired infections --
persists in a variety of different environments.
P. aeruginosa is a remarkably adaptable
bacterium. It naturally occurs in soil and freshwater, but it can also thrive
on the moist surfaces of medical equipment, leading to opportunistic infections
of immunocompromised or otherwise vulnerable patients that result in
life-threatening conditions like pneumonia or sepsis.
One reason for P. aeruginosa's adaptability is its capacity to survive sudden
changes in the water content of its environment.
Rainfall, for example, poses a problem for bacteria because it dilutes the
cell's surrounding media, prompting water to enter the cell by osmosis. Such
"osmotic downshocks" can cause cells to swell up and burst, but some
bacteria, including the gut bacterium Escherichia coli, carry mechanosensitive
channels in their cell membranes that open up as soon as the cell starts to
swell, letting small solute molecules -- or osmolytes -- exit the cell so that
the osmotic gradient driving water influx is reduced. E. coli carries two types
of mechanosensitive channels. The MscS channel releases modest amounts of
osmolytes when swelling causes low amounts of membrane tension. The MscL
channel is activated at higher tension levels to release osmolytes in larger
amounts.
The researchers determined that P. aeruginosa expresses one MscL- and
two MscS-type channels. The MscL-type channel predominates and is present at a
higher density in P. aeruginosa membranes
than its equivalent in E. coli membranes, allowing P. aeruginosa cells to release larger amounts of osmolytes. But the
two MscS-type channels are also important; they are activated earlier in
response to cell swelling, and, by releasing modest amounts of osmolytes, they
can reduce membrane tension and prevent the MscL channels from releasing more
osmolytes than necessary.
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Posted by Dr. Tim Sandle
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