Evolutionary change by means of Natural Selection needs a couple of things in order to happen: heritability and variation in fitness. That is, offspring need to resemble their parents at least a little (heritability) and individuals need to differ in their survival and offspring production (fitness). We’ll worry about heritability in another post, but variation is something that seems like it might be hard to maintain. Some forms of Natural Selection will reduce variation as more fit individuals become frequent and all the different kinds of less fit individuals are eliminated from the population. However, there is a force, common in nature, which may maintain variation, parasites.
Interactions between hosts and parasites can generate strong selective pressures on each player, especially if your life depends on infecting a host. Often, biologists make an analogy to an arms race where players are developing bigger and better defenses or weapons. Antagonistic interactions may also generate negative frequency dependence where a rare host type is favored because the parasites are adapted to a common type. You can learn more by checking out two posts over at Nothing in Biology makes Sense (CJ’s post on the Red Queen Hypothesis or Jeremy’s post on a different coevolutionary puzzle). A key component for maintaining variation via negative frequency dependent selection is specificity. There must variation in the interaction among different host genotypes and parasite genotypes. This is sometimes referred to as a GxG interaction. If parasites can infect all the hosts, there is no specificity. Specificity allows different hosts to be favored over time depending on the composition of the parasite population.
Theoreticians love to use different models of interactions between hosts and parasites, but without empirical evidence, there seems little point. In a recent paper by Rouchet and Vorburger (2012), the authors looked for evidence of just the kind of genetic specificity would result in the maintenance of genetic variation.
|A winged adult aphid being attacked|
by two wasp parasitoids. Photo
by Christoph Vorburger.
Biological system: The Vorburger group studies a crop pest aphid, Aphis fabae, and its common wasp parasitoid, Lysiphlebus fabarum. The adult parasitoids lay their eggs in unsuspecting aphid hosts. As the parasitoids develop they battle the hosts defenses. Some aphid hosts are also infected with a bacterium symbiont, Hamiltonella defensa, which can provide protection against the parasitoid by releasing bacteriophages that target the parasitoid invader (Vorburger et al 2009; Vorburger and Gouskov 2011). If the wasp parasitoid can evade all the host defenses then eventually it develops inside the still living aphid. Eventually, as the authors describe in grisly detail
“metamorphosis takes place within a cocoon spun inside the host’s dried remains, forming a ‘mummy’ from which the adult wasp emerges” (Rouchet and Vorburger 2012).
In order to test the ability of particular parasitoid genotypes to infect hosts, you need a clever trick to generate replicates. Just like Star Wars, the authors act as the benevolent New Republic and generate a clone army of parasitoids. They also generate a series of clonal lines for the hosts as well. They are able to accomplish this feat because both species sometimes use parthenogenesis to produce offspring without fertilization instead of the common sexual reproduction. With parthenogenesis, mothers produce offspring with only their genetic material.
Experiment: The authors created 15 different host lines, most of which were naturally infected with the protective symbionts (more on this bit later). They infected each of these host lines with three different parasitoid clones in a fully crossed design (45 separate comparisons).
Key result: Rouchet and Vorburger (2012) demonstrate that there is variation in the infectivity of the parasitoids clones and this was dependent on the host lines with a significant interaction. This interaction term in their statistical analysis is evidence of the specificity of the infection and defense.
In building up this experiment, the authors include natural infections of the defensive symbiont. In doing so, as the authors point out themselves, the host-symbiont genotypes become confounded statistically. Therefor, the specificity of infection ability of the different parasitoids may be the result of interactions not with the host genome, but with the symbiont genome. However, Rouchet and Vorburger suggest that there is a strong amount of vertical transmission of the symbiont making its genome heritable as well as generating a shared fitness among host and symbiont. Previously, this same group looked for specificity in of the same host-parasitoid interaction using hosts that lacked the symbiont. That research (Sandrock et al 2010) did not find any evidence of the genotype-by-genotype specificity found in this experiment. This further supports their conclusion that the aphid defense is the result of the particular symbiont strain they carry.
In order to develop a causal link that aphid (host) defense is mediated by the symbiont, the authors propose that the next logical experiment would be to cure the aphid lines of the symbiont, ridding the hosts of their protection. If the symbionts are the mechanism generating the specificity of protection from the parasitoids, then we would expect to see increased infection rates and a lack of genotype by genotype interaction, no specificity. The Vorburger research group has already done some of this research by looking at experimentally infected aphids in a paper from earlier this year (Schmid et al 2012). You can read more about that specific paper over at the Parasite of the Day blog by Tommy Leung.
In addition to all the cool empirical work, this research group is also generating some interesting simulations looking at different models of genotype interactions among hosts and parasites that may not fit the typical ones often use by theoreticians (Kwiatkowski et al 2012).
Rouchet R, Vorburger C (2012) Strong Specificity in the Interaction between Parasitoids and Symbiont-Protected Hosts. Journal of Evolutionary Biology: early view. DOI: 10.1111/j.1420-9101.2012.02608.x
Kwiatkowski M, Engelstädter J, Vorburger C (2012) On Genetic Specificity in Symbiont-Mediated Host-Parasite Coevolution. PLoS Comput Biol 8: e1002633. DOI: 10.1371/journal.pcbi.1002633
Sandrock C, Gouskov A, Vorburger C (2010) Ample Genetic Variation but No Evidence for Genotype Specificity in an All-Parthenogenetic Host–Parasitoid Interaction. Journal of Evolutionary Biology 23: 578-585. DOI: 10.1111/j.1420-9101.2009.01925.x
Schmid M, Sieber R, Zimmermann Y-S, Vorburger C (2012) Development, Specificity and Sublethal Effects of Symbiont-Conferred Resistance to Parasitoids in Aphids. Functional Ecology 26: 207-215. DOI: 10.1111/j.1365-2435.2011.01904.x
Vorburger C, Gouskov A (2011) Only Helpful When Required: A Longevity Cost of Harbouring Defensive Symbionts. Journal of Evolutionary Biology 24: 1611-1617. DOI: 10.1111/j.1420-9101.2011.02292.x
Vorburger C, Sandrock C, Gouskov A, Castañeda LE, Ferrari J (2009) Genotypic Variation and the Role of Defensive Endosymbionts in an All-Parthenogenetic Host–Parasitoid Interaction. Evolution 63: 1439-1450. DOI: 10.1111/j.1558-5646.2009.00660.x
Rouchet R, & Vorburger C (2012). Strong Specificity in the Interaction between Parasitoids and Symbiont-Protected Hosts Journal of Evolutionary Biology DOI: 10.1111/j.1420-9101.2012.02608.x