A tiny worm has developed a compelling system for survival: It avoids trouble and sickness. A single genetic change in the tiny worm Caenorhabditis elegans compels some worms to stay away from harmful bacteria and others to eat the microorganisms [Science News]. While some researchers believe that the healthier worms also have some innate immunity to the bacteria, a new study shows definitively that a gene controls their behavior and keeps them from ingesting substances that will do them harm.
As reported in Science [subscription required], researchers first noted that a Hawaiian population of C. elegans had less resistance to harmful bacteria than the standard laboratory worms. A genetic study revealed that the Hawaiian worms have a different version of a gene called npr-1, which causes them to produce less of a protein that senses signals from neurons. When researchers tweaked the standard lab worms to have the same npr-1 mutation, those worms were also more susceptible to infection, indicating that the single gene was somehow responsible.
When the researchers replaced all the worms’ usually innocuous bacterial grub with a small lawn of harmful bacteria, the Hawaiian worms and the npr-1 mutant lab strain worms both gravitated to and ate the pathogenic bacteria, resulting in a high death rate. In contrast, the nonmutant lab strain worms avoided the bacteria and survived longer [Science News]. Researchers marked the bacteria with a green fluorescent protein to see how much of the bacteria each type of worm ingested, and in the images the guts of the Hawaiian worms glow bright green.
In another experiment, researchers spread the harmful bacteria throughout the worms’ environment so that it was unavoidable; in this scenario, the death rates of the two types of worms were the same. Lead researcher Dennis Kim says this proves that the standard lab worms’ health in previous experiments was entirely due to their behavior, rather than the strength of their immune system.
However, geneticist Alejandro Aballay, who has also studied C. elegans and its response to dangerous bacteria, believes that the new research may be overstating the case. Kim’s team found that behavioral responses alone could explain the differences in npr-1 expression and pathogen susceptibility, while Aballay’s team implicated immune effects, too. “Behavioral responses cannot account for all the differences we see,” said Aballay [The Scientist].
Image: Science / Reddy et al.