Spider venom mix-up could make insecticides safer
Thanks to a shipping mistake, scientists have stumbled onto a surprise finding about spider venom and how it can kill one cockroach species without harming a closely related one.
That suggests insecticides could be designed to target specific pests without harming beneficial species like bees.
“Most insecticides used today take a carpet-bombing approach, killing [bugs] indiscriminately and sometimes even hurting humans and other animals,” says Frank Bosmans of the Johns Hopkins University School of Medicine. “The more specific a toxin’s target, the less dangerous it is for everything else.”
Bosmans, an assistant professor of physiology, and his team published their results in the journal Nature Communications.
Desert bush spider
The scientists use spider toxins to study how nerve cells use openings called sodium channels to send out electrical signals. Their unexpected finding began with the mistaken inclusion of a protein, called Dc1a, in a shipment sent to the Bosmans lab by Australian collaborators.
The protein had been extracted from the venom of the desert bush spider Diguetia canities, which lives in the deserts of the southwestern United States and Mexico and is harmless to humans.
When the Australians tested the effect of Dc1a on proteins from American cockroaches, the proteins reacted very weakly, so they hadn’t planned to send Dc1a to Bosmans for further study. But it was accidentally included with other spider venom proteins, so Bosmans’ group decided to test it, he says.
Because his lab recently had acquired the gene for the German cockroach sodium channel, Bosmans’ team tested Dc1a on that protein and saw a startling increase in the channels’ activity, completely different from what happened with the protein from American cockroaches.
“Sodium poured into the cells. In a bug, that would cause massive seizures, much like being electrocuted,” Bosmans says. “Luckily, the toxin doesn’t act on human sodium channels.”
Just two amino acids
Curious about the difference between the two cockroaches’ sodium channels, the researchers first identified the region of the channels that the toxin targets; it turned out to look exactly the same in each species.
Digging deeper, they found a region nearby that differed in the German and American bugs by just two amino acids, the basic building blocks of proteins. When mutations were made in the German version so that its amino acids were the same as the American, the German cockroach sodium channel reacted like the American one.
That confirmed that the tiny amino acid difference was the reason the German cockroach species would succumb to the poison while the American would likely survive.
The team’s next step is to test the toxin on other insect species to determine its full range. Now that they know how important this region of sodium channels is, Bosmans says, researchers will know to look for mutations there.
In addition to the possibility of improved, more specific insecticides, they will be trying to find the mechanism for various human disorders. It may also be possible to create drugs that calm down overactive sodium channels.
Bosmans’ study coauthors are from Johns Hopkins, the University of Queensland, and the University of Technology, Sydney. Grants from the Australian Research Council and the US National Institute of Neurological Disorders and Stroke supported the work.
Source: Johns Hopkins