How gut bacteria controls gene expression through “interspecies communication”

New research reveals insight into how our gut bacteria may changing the way genes are expressed...
New research reveals insight into how our gut bacteria may changing the way genes are expressed in their hosts(Credit: kjpargeter/Depositphotos)

Imagine a tiny microbe living inside you with the power to control the activity of your DNA. Scientists are increasingly discovering how much control our gut bacteria may actually have over us, with a new study describing how individual bacteria can secrete a molecule that literally turns genes off or on.

Epigenetics is a field of study looking at what mechanisms turn specific genes on or off. Separate to our hard-coded DNA, certain external influences can either enhance the expression of a gene or silence it altogether. We know that gut bacteria can modulate the expression of certain genes, potentially influencing the onset of a variety of autoimmune diseases. However, it is unclear exactly how these tiny microbes actually do this.

A fascinating new study has revealed for the first time that certain bacteria can secrete a compound called nitric oxide which is known to regulate gene expression. The researchers describe this interaction between host and bacteria as a form of “interspecies communication.”

Nitric oxide is a gas molecule fundamental to cellular signaling and health. It was only recently, back in 2013, that scientists discovered the molecule’s epigenetic role. The new research set out to understand whether bacteria uses this same network to alter its hosts DNA.

The study used C. elegans worms to examine how this process could work. The worms were administered bacteria known to produce nitric oxide and then the researchers set their focus on a specific protein called ALG-1. This protein is known to play a crucial role in controlling the expression of several genes.

The study revealed that when the bacteria produced excessive volumes of nitric oxide it fundamentally impaired the function of ALG-1 and disrupted the worm’s healthy development. The worm essentially grew deformed reproductive organs and died.

Jonathan Stamler, senior author on the new study, suggests in the real world such an extreme outcome would not pragmatically happen. It’s obviously not in the best interests of either the host or the bacteria to stimulate a biological mechanism that would cause both organisms to die.

“The worm is going to be able to stop eating the bacteria that make the nitric oxide, or it will begin to eat different bacteria that makes less nitric oxide, or change its environment, or countless other adaptations,” says Stamler. “But by the same token, too much nitric oxide produced by our microbiome may cause disease or developmental problems in the fetus.”

As with much microbiome research these days, the study raises more questions that it answers, and it is not entirely clear how this specific mechanism can be harnessed into a useful clinical treatment. Stamler suggests that now this mechanism has been identified, researchers can potentially home in on specific human health outcomes it may be influencing. From that point, future treatments could conceivably modulate this nitric oxide pathway in the gut to benefit human health.

“I now think of this therapeutically, as a drug,” says Stamler. “There are tremendous opportunities to manipulate nitric oxide to improve human health.”

The new study was published in the journal Cell.

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