Products of genes linked to the syndrome coordinate mobile, cargo-carrying motor proteins within the cilia, tiny hairs found on the surface of cells, according to graduate student Guangshuo Ou, postgraduate researcher Joshua Snow and Jonathan Scholey, professor of molecular and cellular biology at UC Davis, and postdoctoral researcher Oliver Blacque and Professor Michel Leroux at Simon Fraser University.

Cilia are found on cells throughout the body, from the retina of the eye to the nose, lung and kidneys, said Ou, who is first author on the study. A variety of human diseases have been shown to be directly linked to defects in cilia, he said. The structure of cilia has been preserved across hundreds of millions of years of evolution -- allowing researchers to study essentially the same genes in an animal as simple as the soil roundworm, Caenorhabditis elegans.

Scholey's laboratory at the UC Davis Center for Genetics and Development uses the worms to directly observe the movement of motor proteins in cilia. The worms have cilia-coated cells in sensory pits near their mouths. Without functioning cilia, they lose their sense of smell.

The cilia are built and maintained by a system of motor proteins called kinesins that carry material from the base to the tip, walking along a protein microtubule. Two different kinesins, Kinesin-II and OSM-3, are required for efficient transport.

By studying worms lacking specific genes, the researchers showed that two genes associated with BBS, BBS-7 and BBS-8, and a third called DYF-1, allow the motor proteins to work together.

"They act as regulators of this subtle coordination," Scholey said.

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If they feel they are sufficiently numerous, they produce two virulence factors, molecular weapons known as PA-I and Pyocyanin. PA-I causes the barrier cells that line the host's bowel to become more permeable, which renders them more susceptible to the microbe's toxins. Pyocyanin enhances the germ's ability to pass through the weakened bowel wall, enter the bloodstream and invade tissue.

"Our goal," Alverdy said, "is to understand the many steps in this process and use that knowledge to find novel ways to intervene, to stop the infection before it starts rather than trying to kill all the germs."

Many harmful bacteria have already learned how to resist the drugs developed to treat them. Scientists are now looking at alternatives, such as ways to block or scramble the chemical messages that allow microbes to eavesdrop on their hosts or to conspire together to mount an attack.

"We chose to study this in Pseudomonas because it is one of the deadliest infections for patients who undergo major surgery," said Alverdy. "We suspect something very similar, however, occurs in all sorts of infections."

Inflammatory bowel disease patients, for example, have elevated cytokines “ the chemical messengers that trigger an immune response “ in the bowel. "These could signal the bug," said Alverdy, "then the bug strikes back and then the inflammation process snowballs." Because the bacteria in this case are "normal flora," people with no real infection develop a chronic disease.

The battles between pathogens and their hosts have been going on for millions of years, Alverdy said, with each side constantly devising novel measures, countermeasures, and counter-countermeasures, including sophisticated mutual espionage.

The discovery of antibiotics gave human hosts a temporary advantage, "but that seems to be waning a bit," he added. "We need to learn new ways to understand our germs and think about how to placate rather than annihilate them."

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