Rational exuberance

August 21, 2009 • 11:40 am

by Greg Mayer

Continuing with the frog theme, here are two representatives of Dendrobates pumilio, the strawberry poison dart frog, from Costa Rica.

Dendrobates pumilio from Estacion Biologica La Suerte, Costa Rica
Dendrobates pumilio from Estacion Biologica La Suerte, Costa Rica
Dendrobates pumilio from Estacion Biologica El Zota, Costa Rica.
Dendrobates pumilio from Estacion Biologica El Zota, Costa Rica.

As the word “poison” in their vernacular name indicates, these frogs are toxic, and their bright coloration is aposematic: it advertises the toxicity of the frog, and protects them from predators. They may often be seen wandering boldly about the rain forest floor in daylight. These two individuals show much of the range of color variation in the species:  red backs with more or less darker speckling, and blue on the extremities ranging from the whole limb to just a hint on the toes and vent.

In northwestern Panama, however, in the region of Bocas del Toro, there are many color morphs– yellows, blues, blacks, greens– some of which are cryptic (i.e. camouflaged), rather than aposematic. In a paper last year (abstract only), Ian Wang and Brad Shaffer of UC-Davis studied the within-species phylogeny of these color morphs, and found that apparently cryptic forms had arisen multiple times. They proposed that this convergence in coloration might be driven by selection. But they admit much more work must be done:

The dramatic level of color polymorphism in the Bocas del Toro populations of D. pumilio remains difficult to explain, especially because our phylogeographic study of color evolution indicates a complex history of color changes.

10 thoughts on “Rational exuberance

  1. These instances are where you do worry that evolution might “explain too much,” as in, if poisonous species are bright they’re aposematic, if they’re camouflaged they’re just hiding. The real point, however, is that evolution is very complex and a great deal of work is needed to study these issues (and money for it isn’t exactly enormous).

    More important than distinguishing between causes of aposematism and cryptic forms would be, I think, figuring out how aposematism itself arises. Why a red body warns animals away in the first place doesn’t seem clear, unless poisonous fruits or insects of similar colors perhaps preceded such colors in amphibians.

    Do our primate relatives seem to understand that bright frogs/toads are not to be eaten? Because it doesn’t seem to me that we naturally understand this to be the case.

    Glen Davidson
    http://tinyurl.com/mxaa3p

    1. Glen, I think it is simply this:

      “I ate a frog and I got so sick that I will never again eat another bright red raspberry frog again!”

      Or the alternative…

      “My cousin ate…”

  2. Based on the antibiotic peptides (magainins) from African clawed frog (Xenopus laevis) skin, I thought surely the poison dart frog toxins would be peptides too, but they’re apparently small-molecule alkaloids: http://en.wikipedia.org/wiki/Poison_dart_frog

    It’s unclear from skimming a few sites whether an individual species produces multiple alkaloids, but this is apparently the most toxic of them all: http://en.wikipedia.org/wiki/Batrachotoxin

    1. The alkaloids on poison dart frogs’ skin are produced from formic acid in their diet – from ants. The antibiotics on African clawed frogs are most likely non-dietary and produced in a different way. That could explain why the compounds are so different. Frogs also produce fungicides and all sorts of compounds on their skin. The permeability of their skin makes them very susceptible to disease, so they need another defense. When frog species go extinct we are losing out on discovering useful substances for medicine.
      I’ve heard that this frog may also come in purplish hues.

      1. The biosynthetic path of these frog toxin alkaloids must be quite interesting. Over half of the batrachotoxin molecule is clearly steroid-derived, which must come from the frog, but (guessing here) if they can’t use their one-carbon metabolism machinery at a key place in making the whole molecule, I could see how dietary formate might be involved.

        I’ve seen reference to the batrachotoxin source being dietary in many links but without further details. Here’s a link to an abstract giving support to a dietary component, along with other related titles: http://www.sciencemag.org/cgi/content/abstract/208/4450/1383 (Frogs captured from the wild retain the toxin for at least 6yrs, but frogs reared in the lab are nontoxic at maturity.) Presumably there’s been considerable further work on this since 1980, but no time right now to chase those.

        The peptide antibiotic magainins are genomically-encoded ~23-residue peptides, synthesized in the usual ribosomal manner as larger precursor forms that are proteolytically cleaved to yield the active peptide – here’s a great review article which seems to be freely available in its entirety: http://www.nature.com/jid/journal/v111/n5/full/5600171a.html

        For non-ribosomally synthesized peptide toxins, the mushroom toxin phalloidin is a great example. It’s cyclic with a fascinating internal cysteine-to-tryptophan crosslink, and contains at least one amino acid not found in ribosomally-synthesized proteins.

      2. It couldn’t just be formic acid – alkaloids have to have a nitrogen atom and formic acid is just HCOOH. To play a role, there’d have to be something wrong with the one-carbon metabolism of the frogs. But see Ray Moscow’s interesting comment on the newer frog posting – they’re apparently assimilated intact, from mites!

        Meanwhile, here’s a great review article on antimicrobial peptides, and it seems to be freely available in toto: http://www.nature.com/jid/journal/v111/n5/full/5600171a.html (all are genomically encoded, ribosomally synthesized, as precursors which then have a neutralizing leader sequence clipped off to yield the active peptide).

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