These Toxic Critters Have Evolved a Surprising Way to Avoid Poisoning Themselves

To discourage predators from playing with your cousins and you, you can make yourself sick by smothering yourself in deadly poison. This genius plan has one flaw. It involves you slathering your self in deadly poison. Toxic compounds can often wreak havoc on enzymes or receptors, so it is smart to create a new set to your deadly keys. However, this doesn't appear to be the way evolution chose for amphibians and birds that produce batrachotoxin. Researchers at the University of California, San Francisco and Stanford University suggested that these animals could instead protect themselves against the toxin's harmful effects by using a protein to absorb it before it causes any problems. This discovery is not only a useful insight into the evolution of toxic defense strategies, but it could also be used to inspire new antidotes for poisonous substances. Batrachotoxin, a neurotoxin, is made from an alkaloid that certain beetles produce. The alkaloid is not a problem for a few bird species in Papua New Guinea, such as the Pitohui, and other poison dart frogs endemic in tropical forests of Columbia. Consuming the beetles gives them a toxic boost. According to some estimates, the golden poison frog Phyllobates terribilis releases about a milligram worth of batrachotoxin from its skin's glands. Although it might not seem like much, it would be enough to send a dozen people into an early grave. It's not only humans that should be concerned. The toxin binds to sodium channels, which control nerve impulses. It can kill almost anything with nerves or a heartbeat. It is obvious that it doesn't block sodium channels in the poison dart frogs and Papuan birds. It is easy to conclude that their sodium-shunting protein are in the wrong form. Studies in the past have identified candidate mutations that could be responsible for this immunity. "However, there haven't been any functional studies of poison frog or Pitohui sodium channels, so whether batrachotoxin-bearing animals rely on changes within their sodium channels or alternative resistance mechanisms remains unclear," says Daniel L. Minor, Jr, a biochemist from the University of California, San Francisco. This team began to fill the knowledge gap by studying and cloning voltage-gated sodium channels in Pitohui uropygialis, a bird that is able to transmit batrachotoxin, and in two poison dart species of frogs. The candidate variant in sodium channels provided poor protection. It doesn't provide a high level of resistance and it doesn't work well in their nerves, as a sodium channel. Minor says that "all of our observations support the hypothesis that sodium channel mutation may be the batrachotoxin authoresistance strategy to poisonous birds and poisonous frogs like P. terribilis." The researchers concluded that there must be a way to intercept the toxic molecules and target the sodium gates before they can be targeted. The toxin was not able to cause any symptoms in the frogs even after they were injected with it. Although the study does not identify any toxic sponges, it is still a significant discovery. A minor previously discovered American bullfrog (Rana catesbeiana), produced proteins that protected against the deadly neurotoxins made by cyanobacteria. It is also known as saxiphilin. It binds with saxitoxin, rendering it ineffective. This could help the frog survive amid algal blooms. It is not yet clear if a similar protection is in place inside Pitohui and poison dart frogs. Minor and his coworkers will investigate the matter. Minor says that these sequestration strategies could not only provide a broad means of toxin prevention but could also be used in pathways involved with safely transporting and concentrating toxic substances in key defense organs like the skin. "Understanding these pathways could lead to the discovery antidotes for various toxic agents." This research was published by the Journal of General Physiology.

0 Comments

Post a comment

Your email address will not be published. Required fields are marked *

0 comments