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Because a solitary bacterial cell can sense its own signaling molecule to reprogram itself from benign to virulent, "quorum sensing" may be a misnomer, according to researchers in New Mexico.
This genetically programmed shift, which on a larger scale typifies quorum sensing within a colony of bacterial cells, can also go forward when a lone Staphylococcus aureus cell is being held within a miniscule reaction vessel.
Those vessels consist of porous silica nanostructures. When mixed with bacteria, the nanostructures form compartments around individual cells, according to materials scientist Jeffrey Brinker and his collaborators at Sandia National Laboratory in Albuquerque, N.M. Before dabbling with intact bacterial cells in these compartments, he and his colleagues were studying how phospholipids reconfigure these inorganic nanostructures. However, that earlier project is taking a back seat to a newer set of microbial experiments, according to Brinker. "Being able to isolate cells made me think about cellular communication," he says. By isolating single bacterial cells within individual nanocells, "we could ask fundamental questions about how quorum sensing works."
Brinker teamed up with microbiologist Hattie Gresham at the University of New Mexico in Albuquerque and her collaborators. They reported in 2008 that apolipoprotein B upsets the quorum sensing signaling cascade in S. aureus (Cell Host Microbe 4:555- 566, 2008), a phenomenon that applies to bacterial cells in dense populations. Brinker, Gresham, and their collaborators wondered what would happen when this disrupting agent was applied to individual cells.
To find out, the researchers encapsulated individual S. aureus cells in silica nanospheres about 20 μm in diameter. An S. aureus cell "builds it own isolation chamber from lipids and soluble silicon dioxide precursors in an evaporating droplet [and then] becomes incorporated with nutrients in an endosomal-like compartment surrounded by a lipid/silica nanostructure," Brinker says. "This construct ensures that each cell is isolated physically and chemically from other cells, while the nanostructured matrix keeps the cells from drying out. Within this confined environment, the increasing concentration of signaling molecules [induces] genetic reprogramming."
To detect what happens within individual cells, the researchers fused the gene encoding green fluorescent protein (GFP) to that for α-hemolysin, a bacterial toxin that is made in response to quorum sensing signal molecules. After signaling begins, GFP (and α-hemolysin) levels in encapsulated cells increase for 10 hours, similar to what happens in ordinary bacterial cultures during quorum sensing. However, because apolipoprotein B disrupts quorum sensing, adding it blocks GFP-α-hemolysin production for about 10 hours. Details appear in the January 2010 Nature Chemical Biology (6:41-45).
The prevailing view of quorum sensing holds that colonies of bacteria containing millions of cells depend on signaling molecules to assess their density and coordinate cooperative behaviors. Whether a solitary bacterium is even subject to quorum sensing was never before tested, according to Rose Redfield of the University of British Columbia, Vancouver, Canada. The findings of Brinker, Gresham, and their collaborators "now provide definitive evidence that isolated cells can benefit from sensing the autoinducer molecules they themselves secrete," she says. Several years ago Redfield postulated that autoinducers might enable individual bacterium to sense properties within their microenvironments. However, she says, "I couldn't think of a way to demonstrate this."
Quorum sensing is "an eye-catching term, but it limits your view of biology," says microbiologist Michael Federle from the University of Illinois, Chicago. Infections by Streptococcus pyogenes, the pathogen that he studies, might start with a small number of cells or only one. Understanding how cell-cell communication might sometimes impede-instead of foster-the development of virulence could prove clinically valuable, he points out. Brinker and Federle belong to an informal group whose members focus on similarities between quorum sensing and cancer metastasis. For example, cancer cells are more likely to metastasize if they originate from high-cell-density tumors, according to Federle. Perhaps tumors experience some type of quorum sensing. Learning how cancer cells communicate and overcome immune surveillance "has similarities to how bacteria behave in biofilms or fight the immune system," he says.
Carol Potera
Carol Potera is a freelance science writer in Great Falls, Mont.
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