A genetic mechanism that controls the production of a large spike-like protein on the surface of Staphylococcus aureus bacteria alters the ability of the bacteria to form clumps and to cause disease, according to a new study.
Under
normal conditions, Staphylococcus
bacteria interact with proteins in human blood to form aggregates, or clumps.
This clumping behavior has been associated with pathogenesis -- the ability of
bacteria to cause disease. However, the mechanisms that control clumping are
not well understood.
In
the process of investigating how staph bacteria regulate cell-to-cell
interactions, researchers at the UI Carver College of Medicine discovered a
mutant strain of staph that does not clump at all in the presence of blood
proteins.
Further
investigation revealed that the clumping defect is due to disruption of a
genetic signaling mechanism used by bacteria to sense and respond to their
environment. The study shows that when the mechanism is disrupted, the giant
surface protein is overproduced -- giving the cells a spiny, or
"porcupine-like" appearance -- and the bacteria lose their ability to
form clumps. Furthermore, the research team found that this clumping defect
also makes the bacteria less dangerous in an experimental model of the serious
staph infection, endocarditis.
For
further details, see:
Posted by Tim Sandle
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