How did zootoxins evolve?

Question

I've always wondered how toxins in certain organisms have evolved. Particularly, organisms that produce toxins as a deterrent to predators as opposed to organisms that use it to paralyze their prey. **Where did this toxicity come from? How did it develop to what it is today?** There must've been a drawn out period where evolution 'tested' and 'fine-tuned' the toxin. Presumably until it was somewhat efficacious to the target. What are the current popular theories on this?

Answer 1

Hi there! This question is fantastic – it shows you’re thinking exactly like a zoologist. Like many zoological and evolutionary questions, it doesn’t have a straightforward answer.

One key thing to understand is that natural selection isn’t an active decision-making process. It’s easy to imagine evolution as something intentionally testing traits to see what works, but that is not how it works. Instead, evolution is driven by random genetic mutations. Most mutations do not help the organism, and some may even be harmful. But every so often, a mutation gives an organism a little advantage that helps with survival or reproduction.

You’re asking specifically about defensive toxin – poisons used by animals to keep predators away—rather than offensive toxins used to catch prey. While both types of toxins evolve through natural selection, they’re driven by different selective pressures.

For defensive toxins, the story often starts with a mutation that lets an animal tolerate a toxin. There are a few different ways this can happen.

Biochemical Pathways: A mutation changes a chemical process in the body, causing the production of a toxin. Poison dart frogs are a good example.

Gene Duplication: A gene may duplicate by chance, leading to the creation of a new or overproduced chemical. Some salamanders with toxic skin secretions may have evolved this way from duplication of genes that normally produce their protective skin mucus.

Sequestration: A mutation allows the organism to eat something containing a toxin and store it without being harmed.

For example, some animals (like monarch caterpillars) eat toxic plants like milkweed. A mutation in one ancestor monarch’s DNA might have allowed it to consume the plant without being harmed and store the toxin in its body. That monarch survived a bit longer, had more offspring, and passed the mutation to them. Some of those offspring might have also stored the toxin in their bodies, making them unappetizing to predators.

Even if a bird ate one of these toxic caterpillars and got sick, it would quickly learn to avoid monarchs altogether. So even though a few caterpillars with the mutation might be eaten, others survive and grow up to lay eggs with the same trait. Over generations, this mutation spreads throughout the monarch population—not because the mutation was tested or fine-tuned, but because these animals simply survive and reproduce more successfully.