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Scientists Dissect Bacterial Crosstalk

Date:
August 23, 1999
Source:
Washington University School Of Medicine
Summary:
Please pass the sugar, a hungry bacterium says. And the lining of the intestine complies. But how can microbes talk to mammals' With a dual-purpose protein, scientists find.

St. Louis, Aug. 20, 1999 -- Please pass the sugar, a hungry bacterium says. And the lining of the intestine complies. But how can microbes talk to mammals' With a dual-purpose protein, scientists find.

The microbes in our body -- more numerous than human cells -- fend off pathogens and do other essential chores. "But we know very little about how our relationships with them are forged," says Jeffrey I. Gordon, M.D. "We want to understand the conversations that occur between these microbial guests and their host."

The findings appear in the Aug. 17 Proceedings of the National Academy of Sciences. Gordon, the Alumni Professor and head of molecular biology and pharmacology and professor of medicine at Washington University School of Medicine in St. Louis, is senior author of the paper. Postdoctoral fellow Lora V. Hooper, Ph.D., is first author.

Four hundred species of microbes call our gut home, competing for space and food. To cut through the cacophony, the researchers studied just one species.

Bacteroides thetaiotaomicron lives in the lower part of the gut and feeds on a sugar called fucose. It arrives early in a mammal's life, paving the way for other friendly microbes.

Using germ-free mice, Gordon's group previously showed that cells lining the intestine make fucose, posting the sugar on the cell surface. At weaning, fucose production stops. But it starts up again if mice are exposed to B. thetaiotaomicron. So the bacterium somehow tells the intestine to give it food. And the researchers have found the molecular switch.

First, Hooper created mutants of B. thetaiotaomicron that were unable to utilize fucose. Analyzing these strains, she identified five genes in a row that shared a regulatory region.

Four were involved in fucose uptake or metabolism. But the first coded for a repressor protein, FucR. Hooper purified the repressor and studied FucR mutants. She deduced that the protein halts the transcription of the five genes by interacting with the common regulatory region. But when fucose is available, it no longer can bind to that spot on the DNA. So the bacterium can make the enzymes that metabolize fucose.

Bacteria frequently employ this type of regulation. But B. thetaiotaomicron uses the repressor to tie ordering to inventory.

To see how the bacterium communicates with intestinal cells, Hooper infected mice with various B. thetaiotaomicron mutants. Those that were unable to make fucose isomerase, the first enzyme in the fucose-metabolizing pathway, couldn't tell the mice to give them fucose. But mutants that were unable to make FucR had no trouble getting this message across, even though they didn't make fucose isomerase. So fuculose, the substance made by the isomerase, isn't the give-me-fucose signal.

The researchers proposed a different explanation. They suggest that FucR interacts with the regulator of at least one other gene, which they call csp (control of signal production). When the repressor silences csp, the bacterium stops talking to the intestine. When the repressor is absent, signaling proceeds. "So FucR is the key switch that determines whether the bacterium consumes fucose or asks for more fucose," Gordon says.

FucR's dual function depends on its ability to interact with fucose, the researchers suggest. Although the sugar allows the repressor to switch on the production of fucose-metabolizing enzymes, it enables it to switch off the signal to the intestinal cells.

If the bacterium contains plenty of fucose, most of its FucR will be attached to sugar. So the repressor will be powerless to prevent the production of fucose-metabolizing enzymes. But FucR will bind to the regulatory region of csp. So the pass-the-sugar message won't be sent.

If the bacterium runs short of fucose, most of the FucR will lack sugar. So it will switch off the production of fucose-metabolizing enzymes. But it no longer will silence csp, so the request for fucose will go forth.

Hooper obtained evidence for this model. The mutant that couldn't transport fucose into the cell cajoled mice into making fucose. And the mutant that lacked fucose isomerase signaled once more if the fucose transporter was removed. This type of communication might be too useful to be just an interesting fluke. The paradigm may apply to other nutrients and other forms of requests to hosts, Hooper and Gordon say.

Understanding microbe to mammal communication may help us cope when our friendly bacteria are slain by antibiotics and harmful microbes rush to fill the places at the table. "These messages undoubtedly contribute to the stability of intestinal ecosystems," Gordon says. "So the lessons we learn may help us keep the microbes we need and prevent the encroachment of those we would rather not have."

Grants from the National Institutes of Health supported this research, and fellowships from the Lucille P. Markey Foundation and the National Institutes of Health supported Hooper.

Hooper LV, Xu J, Falk PG, Midtvedt T, Gordon JI. A molecular sensor that allows a gut commensal to control its nutrient foundation in a competitive ecosystem. Proceedings of the National Academy of Sciences 96, 9833-9838, Aug. 17, 1999.


Story Source:

The above story is based on materials provided by Washington University School Of Medicine. Note: Materials may be edited for content and length.


Cite This Page:

Washington University School Of Medicine. "Scientists Dissect Bacterial Crosstalk." ScienceDaily. ScienceDaily, 23 August 1999. <www.sciencedaily.com/releases/1999/08/990823071819.htm>.
Washington University School Of Medicine. (1999, August 23). Scientists Dissect Bacterial Crosstalk. ScienceDaily. Retrieved July 26, 2014 from www.sciencedaily.com/releases/1999/08/990823071819.htm
Washington University School Of Medicine. "Scientists Dissect Bacterial Crosstalk." ScienceDaily. www.sciencedaily.com/releases/1999/08/990823071819.htm (accessed July 26, 2014).

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