Moonlighting Squid Helps Quest for Superdrugs

Scientists say they have found a key gene in a bacterium that lives in a tiny glowing squid that opens up an intriguing conceptual path in the quest for next-generation antibiotics.

The switch reveals a bacterial pressure point that can be attacked in germs that make us sick, they hope.

The researchers focused on a bacterium called Vibrio fischeri that lives peacefully in a diminutive Pacific creature, the bobtail squid (Euprymna scolopes).

The squid feeds at night near the ocean surface and uses a strain of V. fischeri in its light organ in order to mimic moonlight. The gentle glow acts as a cloaking device to protect the squid from predators below.

The investigators pored over the genome of the squid’s variant of V. fischeri and compared it with a V. fischeri which lives in a very different host.

This is the pinecone fish, a small reef fish that uses the germ in a light organ in its jaw. Like a flashlight, the glow enables the fish to forage for food at night.

What the team were looking for was the tiny but essential difference between the strains that had enabled the bacterium to hole up happily in two very different species of animal.

Most of the bacterium’s genome was amazingly conserved, pointing to an organism that had been an evolutionary success for millions of years.

The distinction, though, was that the squid’s version of V. fischeri had a “regulatory” gene that was not present in the fish’s.

This gene acted like a switch. It turned on other genes that then lay down a biofilm enabling the microbe to colonise the squid’s light organ.

The finding is important because human beings, like all forms of life, live in coexistence with bacteria.

These germs are drawn from the environment and inhabit our bodies and perform useful tasks, such as converting food to energy or protecting us from disease, said microbiologist Mark Mandel of the University of Wisconsin at Madison, who led the research published in the journal Nature.

But some strains of these germs are nasty — or can become that way.

One such example is the intestinal germ Escherichia coli, said co-author Ned Ruby.

“With E. coli, you can go from being a beneficial or benign micro-organism in a human to picking up genes that will enable it to become a pathogen,” he said, referring to a potentially lethal intestinal bug.

Pinpointing the regulatory gene that prompts a germ to change from the nice Dr. Jekyll to the evil Mr. Hyde could help the search for treatments that flick the bacterial off switch, he said.

Ruby cautioned, though, that the paper aimed at opening up new horizons in thinking about host germs, and no one should expect such drugs any time soon.

“We’ve been looking too much for evidence of large numbers of genes that move into bacteria and cause pathogenicity,” Ruby told AFP.

“This paper says, ‘Wait a minute. There are actually other ways in which to go to the dark side that are much more subtle and require just a single gene to be moving around.’

“The idea is that you go for just the one gene that’s responsible for regulating a whole series of genes. So long as that regulator is taken out of the picture, it [the bacterium] won’t do anything bad.”

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