Origin Of Mimicry Research Articles

Tracing the origin and evolution of supergene mimicry in butterflies

Supergene mimicry is a striking phenomenon but we know little about the evolution of this trait in any species. Here, by studying genomes of butterflies from a recent radiation in which supergene mimicry has been isolated to the gene doublesex, we show that sexually dimorphic mimicry and female-limited polymorphism are evolutionarily related as a result of ancient balancing selection combined with independent origins of similar morphs in different lineages and secondary loss of polymorphism in other lineages. Evolutionary loss of polymorphism appears to have resulted from an interaction between natural selection and genetic drift. Furthermore, molecular evolution of the supergene is dominated not by adaptive protein evolution or balancing selection, but by extensive hitchhiking of linked variants on the mimetic dsx haplotype that occurred at the origin of mimicry. Our results suggest that chance events have played important and possibly opposing roles throughout the history of this classic example of adaptation.

Mimicry inHeliconiusand Ithomiini butterflies: The profound consequences of an adaptation

Prey populations have evolved multiple strategies to escape predation. Camouflage is a strategy resting on avoiding detection by potential predators, whereas aposematism relies on advertising chemical defences with conspicuous warning signals. While camouflaged phenotypes are subject to negative frequency-dependent selection, aposematic preys are under positive frequency-dependence, where the efficiency of a signal increases with its own local abundance. Because of his “strength-in-number” effect, multiple chemically-defended species exposed to the same suite of predators gain a selective advantage from converging on the same warning signals. Convergence in warning signals is called Mullerian mimicry. Here, we review the results of recent genetic and ecological research on two well-studied groups of neotropical Mullerian mimetic butterflies, the genus Heliconius and the tribe Ithomiini, which advertise their unpalatability through conspicuous wing colour patterns. Mimicry represents a major adaptation in these groups, where the effects of selection extend well beyond mere phenotypic resemblance. Selection acts on other traits used as mating cues, on the genetic architecture of colour pattern and even on the ecological niche of species. The origin of mimicry itself and the coexistence of multiple mimicry patterns are well understood, but the ultimate drivers of mimicry diversity remain unclear.

Batesian Mimicry: Can a Leopard Change Its Spots — and Get Them Back?

Can undefended mimics survive outside the range of their noxious models? Two recent studies on Batesian mimicry suggest they can, but alternative survival strategies and morphologies are then favoured.

Jack-of-All-Trades “Supergene” Controls Butterfly Wing Pattern Diversity

While studying the local flora and fauna of the Amazon jungle in the 1860s, Henry Walter Bates made a striking discovery. Butterflies inhabiting a particular geographic region sported the same wing patterns—even though they were unrelated species. Bates proposed that nonpoisonous species had mimicked the patterns of noxious species that predators avoided, thus gaining a selective advantage. (This adaptation is viewed as one-sided; if predators eat the foul-tasting “model” butterfly, they learn to shun all butterflies with that pattern. But if they sample a palatable mimic, they’re likely to stop avoiding butterflies with that pattern—until they relearn their lesson.) Today, scientists can use the tools of genomics and genetics to investigate the mechanism of convergent evolution—the emergence of similar physical traits (or phenotypes) in unrelated species. Such empirical studies have provided insight into a longstanding controversy spawned by evolutionary theorists over the origin of mimicry: does it arise gradually through the accumulation of random mutations by selection or in “phenotypic leaps” through the constraining influence of shared developmental pathways with a bias toward a particular phenotype? Recent molecular studies found evidence that regulation or recruitment of the same genes or gene variants may explain convergent evolution. In a new study, Mathieu Joron, Chris Jiggins, and colleagues took a different approach by investigating the molecular basis of both convergent and divergent phenotypes. The involvement of the same genomic loci in convergent phenotypes suggests that developmental constraints give rise to these shared phenotypes. The presence of a multitude of convergent and divergent phenotypes in the wing patterns of Heliconius butterflies allowed the researchers to test the possibility that mimetic convergence results from constraints in the regulation of butterfly color patterns. The researchers worked with three species of Heliconius butterflies, including Mullerian mimics (all mimetic species are poisonous, to mutual benefit). Two species, H. melpomene and H. erato, are distantly related yet have identical wing patterns. Both species radiated into over 30 races (or subspecies) in parallel, with the two species (“co-mimics) displaying a single pattern locally. The third species, H. numata, is closely related to H. melpomene but has radically different wing patterns, with up to seven different variations in a single region. Each of these variations mimics a different species of another butterfly genus, Melinaea. In H. melpomene, variation in white and yellow patterns is controlled by at least three genomic loci—N, Yb, and Sb—that are tightly linked, or inherited together. Red pattern elements are controlled by another linked loci pair—B and D. In H. erato, the Cr locus produces patterning effects similar to the interaction of N, Yb, and Sb in H. melpomene, while an unlinked locus, D, appears to control red pattern variation much like the B–D pair does in H. melpomene. In polymorphic H. numata, all the mimicked color patterns derive from a single locus, P, thought to be a “supergene” (a tightly linked cluster of individual genes). The researchers crossed different races of each of the three species to explore the genetic basis of the variations. For example, two different subspecies of H. melpomene from different regions in Ecuador were crossed with an H. melpomene subspecies stock from French Guiana to produce second-generation offspring. Offspring were then genotyped to identify genes responsible for the resulting color patterns and to map the relevant major color-patterning loci—N, Yb, and Sb loci for H. melpomene crosses, Cr for H. erato, and P for H. numata—in individual offspring. Using molecular markers developed in the region of the pattern genes, they found that the three loci controlling color pattern variation for each species inhabit the same genomic location. Indeed, the elements controlling white and yellow pattern variation in H. melpomene (N, Yb, and Sb) and H. erato (Cr) are tightly linked to genetic markers that occupy the same position in both species. Similarly, the locus P, which controls whole-wing variation in H. numata, is also linked to the same series of markers. These results, Joron et al. conclude, suggest that a single conserved locus is responsible for producing wing pattern diversity in Heliconius butterflies. Rather than a constraining role, this locus provides what the researchers call a “jack-of-all-trades flexibility.” It presumably functions as a “developmental switching mechanism” for natural selection, they explain, by responding to a wide range of mimetic pressures to produce radically divergent, locally adapted wing patterns. Now researchers can begin to identify and determine the modus operandi of the genes at the center of what has been called a “developmental hotspot” to better understand how they drive the adaptive evolution of mimetic color pattern shifts. For more on the evolution of mimicry in butterflies, see the Primer (DOI: 10.1371/journal.pbio.0040341 in the October 2006 issue).

Molecular Mimicry of Carbohydrates by Peptides

The use of carbohydrates as drugs and vaccines has several limitations. Molecular mimics of carbohydrates provide an alternative source of compounds to target pathways involving protein-carbohydrate interactions. In recent years, immunological studies have demonstrated the ability of certain peptides to act as molecular mimics of carbohydrates, in that they are able to induce an anti-carbohydrate immune response. Carbohydrate-mimetic peptides that bind to enzymes and lectins have also been discovered. The nature of this mimicry at the molecular level is currently the subject of investigation. Structural data regarding the origin of mimicry are reviewed, and their implications for drug and vaccine design are presented.

Mimicry and the Monte Carlo predator: the palatability spectrum, and the origins of mimicry

With a view to clarifying some recent controversies, the behaviour of a predator confronted with a mixture of models and mimics has been simulated by a simple Monte Carlo computer program. When learning and forgetting are described by a stochastic model in which learning depends on experience, and forgetting on the passage of time, then the ‘spectrum of palatability’ (that is, the continuous variation in the desirability of prey to a predator, from the delectable, through the neutral, to the downright revolting), is converted into a spectrum of protection, in which palatable prey are heavily consumed and distasteful prey are largely avoided. In such a system, a palatable (Batesian) mimic is protected, but causes an increase in the rate of predation on its model (compared with an identical but un-mimicked control); but when both model and mimic are distasteful (Muellerian mimics), both species gain in protection. The mimic in a Muellerian system can be regarded as the species which would be the less protected, and which therefore gains the more from the mimicry. When mimicry evolves by a single large mutation, it is this species which will change: the model will not alter in pattern at this stage. It is useful to recognize a further category, effectively neutral mimicry, in which the mimic, because it is rare or nearly neutral in palatability, has virtually no effect on the model. The fitness of mimics is density-dependent: positively for Muellerian mimics (more protection when common) and negatively for Batesian mimics (more protection when rare). The computer model thus gives results which conform with some of the traditionally accepted differences between Batesian and Muellerian mimicry. It is suggested that warning colour will usually evolve in the form of Muellerian mimicry, or perhaps as Batesian mimicry in species whose behaviour makes them conspicuous, and that distastefulness will usually evolve in cryptically-coloured species. The usual evolutionary pathway to full aposematism is predicted to be distastefulness first and warning colour second.