Tuesday 20 May 2014

Venomous Animals and their Prey

There is a constant tug-of-war between venomous animals and their prey and predators. Most venoms are used for prey capture, and in some species, the venom is targetted towards a specific species of prey. This is seen in a wide range of animals, including spiders, scorpions, cone snails, and snakes. For example, there is a correlation between the diet of Malayan pit vipers (Calloselasma rhodostoma) and their venom. The prey and predators have a evolved a resistance to the venom of these species. The venom resistance in prey and the evolution of novel venom composition exert reciprocal selective pressures on each other, causing both venomous animals and their prey to race to gain the upper hand (Casewell, et al., 2013).

A Malayan pit viper (Image 1).

Venom synthesis appears to carry an appreciable metabolic cost. Some animals display behavioural adaptation to optimise venom expenditure. Rattlesnakes, for example, change the amount of venom that they inject into their prey depending on the size of their prey. Scorpions and spiders inject more venom when the intensity and/or duration of prey movement is increased, or when dangerous prey is encountered (Casewell, et al., 2013).

A rattlesnake (Image 2).

Defence is a common secondary function of venom (in the animals that don't use venom primarily for defence) and animals have defence-specific morphological and behavioural adaptations. There is currently little evidence for defence-related selective pressures on venom composition. Some snakes have evolved to eat undefended prey (such as eggs) or use constriction as prey subjugation, resulting in the disappearance of the venom apparatus and degeneration of toxin genes. This suggests that prey capture is the principal selective force acting on venom and the retention of the venom apparatus (Casewell, et al., 2013).

A snake eating an egg (Image 3).

There is an 'overkill' hypothesis that selection for venom potency is unlikely because the amount of venom injected into prey is often greater than 100 times the lethal dose required. This hypothesis overlooks the fact that laboratory animals might not reflect the response of natural prey to venom. The target-specific venom could be an explanation of why venom is so excessively lethal to labratory animals. Specific venoms have evolved among natural prey and predators, many of which have also evolved a natural resistance to the venom. A variation in venom composition leads to differential venom effectiveness against different prey; therefore, laboratory animals would not have this resistance and the venom would seem to be excessively potent (Casewell, et al., 2013).

References

Casewell, N. R., Wüster, W., Vonk, F. J., Harrison, R. A. & Fry, B. G. 2013. Complex cocktails: the evolutionary novelty of venoms. Trends in Ecology and Evolution 28: 219-229.

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2 comments:

  1. This idea of an evolutionary tug-of-war (arms race) is an interesting one. How much empirical evidence is there really that this is what is happening in these predators and their prey? In populations of prey animals that start to develop resistance, why don’t we get to a point where there is total resistance, or there is such a potent venom that nothing can withstand it? Do you think that runaway selection could possibly explain the potency of some venoms?

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    1. Runaway selection could explain venom potency. It would be interesting if females could pick up on venom potency through a physical or chemical cue.

      The venomous animals might change their target prey (over a large amount of time) depending on population density and size of the prey. This changing relationship could explain why there's no extremely potent venom or extremely resistent prey. Most venomous animals don't only eat a specific species. If their venom targetted one species completely, it might become less potent to other species. Likewise, the prey is probably being attacked by multiple venomous species (especially in Australia where venomous animals are everywhere) and being very resistant to one species might make it more susceptible to another species.

      I can imagine that it would be hard to test whether the evolutionary arm's race is actually occuring. Determining what gene/s codes for the feature would be a challenge, and then monitoring it for decades (or longer) would be difficult.

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