Mutant Dietary Bacteria as a Way to Explore Mechanisms of Aging in Nematodes

Researchers here outline a novel method of searching for longevity-related mechanisms in nematode worms: mutate the bacteria that the worms eat. The researchers worked their way through a selection of bacterial mutations, and along the way uncovered a few items of interest for further exploration. I think the leap made by press and publicly materials to supplements for human consumption containing mutated bacteria is getting far ahead of the science, however. This is, as of the moment, really only a demonstration of a new method of discovery in a commonly used laboratory species.

Scientists have identified bacterial genes and compounds that extend the life of and also slow down the progression of tumors and the accumulation of amyloid-beta, a compound associated with Alzheimer's disease, in the laboratory worm C. elegans. "The scientific community is increasingly aware that our body's interactions with the millions of microbes in our bodies, the microbiome, can influence many of our functions, such as cognitive and metabolic activities and aging. In this work we investigated whether the genetic composition of the microbiome might also be important for longevity."

This question is difficult to explore in mammals due to technical challenges, so the researchers turned to the laboratory worm C. elegans, a transparent, simple organism that is as long as a pinhead and shares essential characteristics with human biology. During its 2 to 3 week long lifespan, the worm feeds on bacteria, develops into an adult, reproduces, and progressively ages, loses strength and health and dies. Many research laboratories around the world work with C. elegans to learn about basic biological processes.

Researchers employed a complete gene-deletion library of bacterium E. coli; a collection of E. coli, each lacking one of close to 4,000 genes. "We fed C. elegans each individual mutant bacteria and then looked at the worms' life span. Of the nearly 4,000 bacterial genes we tested, 29, when deleted, increased the worms' lifespan. Twelve of these bacterial mutants also protected the worms from tumor growth and accumulation of amyloid-beta." Further experiments showed that some of the bacterial mutants increased longevity by acting on some of the worm's known processes linked to aging. Other mutants encouraged longevity by over-producing the polysaccharide colanic acid. When the scientists provided purified colanic acid to C. elegans, the worms also lived longer. Colanic acid also showed similar effects in the laboratory fruit fly and in mammalian cells cultured in the lab.

Interestingly, the scientists found that colanic acid regulates the fusion-fission dynamics of mitochondria, the structures that provide the energy for the cell's functions. "These findings are also interesting and have implications from the biological point of view in the way we understand host-microbe communication. Mitochondria seem to have evolved from bacteria that millions of years ago entered primitive cells. Our finding suggests that products from bacteria today can still chime in the communication between mitochondria in our cells. We think that this type of communication is very important and here we have provided the first evidence of this. Fully understanding microbe-mitochondria communication can help us understand at a deeper level the interactions between microbes and their hosts."



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