When infection is unavoidable, fruit flies ramp up recombination

So, you wanna head back to my place after this and make some recombinant offspring?

Imagine you find yourself in the midst of a large-scale epidemic, similar to the scenarios portrayed in movies like Contagion or Outbreak (or both!). The disease is extremely contagious, and the probability of becoming infected is high. Now imagine that scientists fail to discover a cure. There is no Dustin Hoffman-led team of military virologists available to develop a vaccine and save humanity, and the disease persists, with the potential to infect subsequent generations. In this harsh, disease-ridden environment, how could you ensure that your future offspring would survive?

It turns out, if you were a fruit fly, you might rely on recombination.

Disease is thought to have played a major role in shaping the reproductive strategies of animals. The Red Queen hypothesis predicts that species experiencing parasite-related selection pressures are more likely to evolve sexual reproduction, along with increased rates of outcrossing and recombination. This is because, in the ongoing evolutionary arms race between hosts and parasites, a little bit of genetic variation can make it a lot harder for the parasite to “win.”

But while strategies for increasing genetic variation may improve disease resistance, they often come at a cost. Increased recombination, in particular, can reduce fitness by breaking up locally adaptive combinations of alleles. One potential way to get around this issue is to increase recombination rates only when the risk of infection is high. However, we have yet to observe direct evidence of parasite-induced recombination in animals.

In a study recently published in Science, Singh et al. sought to investigate the capacity of fruit flies to plastically increase recombination in response to infection. To do this, the researchers infected Drosophila melanogaster females with a variety of parasites, and observed the proportion of recombinant offspring the females produced.

In order to track recombination events, researchers took advantage of the known genetic basis of two visible phenotypic traits. The ebony locus and the rough locus occupy nearby positions on the same chromosome in D. melanogaster, and recessive mutations at each of these loci have easily identifiable effects on the phenotype. For this study, the researchers generated females heterozygous at both ebony and rough.

Next, the researchers infected females with one of several different types of parasites. Two distinct (but similarly disturbing-sounding) methods were used to infect flies, depending on the type of parasite involved. In some trials, the researchers stabbed adult flies in the thorax with a needle covered in disease-causing bacteria. In other trials, the researchers housed larval flies with female parasitic wasps, allowing the wasps to inject their eggs directly into the larvae. Seriously, these flies must have been terrified.

A parasitic wasp (Leptopilina heterotoma) probes for fruit fly larvae with her ovipositor.

A parasitic wasp (Leptopilina heterotoma) probes for fruit fly larvae with her ovipositor. (Photo courtesy of Dr. Michael Martin)

Finally, the researchers backcrossed infected females to double-mutant males, and examined the resulting offspring. Sorting through thousands of individual flies, researchers identified recombinant offspring as those that exhibited one mutant trait but not the other.

As predicted by the Red Queen hypothesis, infected females produced significantly more recombinant offspring than non-infected females. The researchers saw this pattern across all types of infection studied, including infection by species that parasitize D. melanogaster in the wild. Furthermore, the effect persisted across host life stages, with females producing more recombinant offspring even when infection occurred during the larval stage of development.

The study also provided some insight on the underlying mechanism for making more recombinant offspring, which – surprisingly – appears not to involve an actual increase in recombination rate. Instead, the culprit looks to be some form of transmission distortion, whereby recombinant gametes are promoted at the expense of non-recombinants.

This study highlights the remarkable ability of individual organisms to rapidly respond to changes in the environment, as well as the central role disease has played in shaping the evolutionary trajectory of animals.

But the reason I’m REALLY excited about these findings is because of their potential to reinvigorate the post-apocalyptic science fiction genre.

Picture this: 50 years after the emergence of an unprecedentedly deadly cross-species pathogen, the majority of the planet’s human population has been wiped out. The only people remaining are the highly recombinant offspring of those infected with (and ultimately killed by) the disease. In a world where survival of the fittest reigns supreme, these exceptionally disease-resistant individuals must attempt to rebuild society as they contend with resource shortages, lawless bands of savages, and the unknown genetic ramifications of the extreme levels of heterozygosity within their population.

It sounds like the beginnings of a pretty solid screenplay to me.

While you’re waiting for my movie to hit theaters, you can read the full text of the Science article here. And check out the video below (courtesy of Dr. Michael Martin), which shows a parasitic wasp female attempting to deposit her eggs in some (probably pretty freaked out) fruit fly larvae.

The Lady Gaga of ferns, and the Spartacus of ants

Friend of the blog (and former contributor) Devin Drown is wrapping up his first year on the faculty of the University of Alaska Fairbanks, where he’s been teaching the Principles of Evolution course. As a final assignment, Devin’s students are contributing posts to a class blog, Evolution, Naturally — and the first couple are great!

Margaret Oliver digs into the phylogenetic data used to support the renaming of a genus of desert-adapted, clonally reproducing ferns — after Lady Gaga. It turns out that the singer’s stage name is literally encoded in the DNA sequence that helps differentiate the new genus from its closest relatives, as Oliver illustrates in the best. Phylogeny. Figure. Ever.

(Evolution, Naturally)

Oliver’s Figure 3. (Evolution, Naturally)

Meanwhile, Alexandria Wenninger explains how some species of ants steal larvae from other ant colonies and raise them as workers — and how entomologists are discovering that those kidnapped workers can resist this unasked-for reassignment.

However, there is a growing body of evidence suggesting that the [captured workers] are not always so oblivious to their origins, as researchers observe more and more situations of what they are calling “slave (host) rebellion”. Czechowski and Godzinska, in their recent review article, “Enslaved ants: not as helpless as they were thought to be”, identify four types of rebelling behaviors, which range from aggressive acts by individual ants to a collective uprising against the parasites.

Feeling a little ill? Blame the trees (not just their pollen either)

A fungus called Cryptococcus gattii, has long known to be infective to humans… even though it’s found on trees.

This has particularly been a problem in Southern California, where people have been getting sick from C. gattii for yeas, and no one knew which tree was harboring the fungus. Find out who the culprit is and how they figured it out! 




Ed Yong on mind-controlling parasites

Here at Nothing in Biology Makes Sense, we’re fascinated by all the weird, baroque ways that living things influence and coevolve with each other—so Ed Yong’s new TED talk about mind-controlling parasites is right up our alley. Just like his writing—currently on display at National Geographic‘s Phenomena, among many other venues—it’s a compendium of nifty natural history punctuated with highly educational gross-outs and the occasional black-belt level pun.

When a bad bird goes good … and then bad again.


Brood parasites are definitely the bullies of the avian world.  They lay their eggs in the nests of other birds, sometimes destroying the host’s own eggs or just waiting for their nestlings to do the dirty work after they hatch.  They then outcompete any surviving host nestlings for food, while the poor host parents are worked to the bone to feed the monstrous nest invader.

In spite of the steep costs of nest parasitism, most avian host species do not have effective mechanisms for detecting and removing brood parasites from their nests.  So, why don’t mama birds notice they have a GIANT intruder in their nest and carry out some infanticide of their own?  One hypothesis is that the cost of a mother bird making a mistake and pushing the wrong baby out (i.e. her own) outweighs the benefit of developing such a behavior.

This week in Science, Canestrari et al. published evidence for another hypothesis – that sometimes, it might actually be good to have your nest parasitized.

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When mummies attack! Why specificity matters for coevolution

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). WORDLE Rouchet Vorburger 2012We’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 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.

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Multidimensional coevolution, no oscillation overthruster required

Gilman etal 2012 wordleConventional wisdom suggests that pathogens and parasites are more rapidly evolving because of various reasons such as short generation time or stronger selection. Yet somehow, they have not completely won the battle against the host. Recently, a theoretical paper on coevolution in Nature caught my eye (Gilman et al., 2012). Here the authors address this paradox: “How do victim species survive and even thrive in the face of a continuous onslaught of more rapidly evolving enemies?

Instead of treating a coevolutionary interaction between two species as the interaction of only two traits, the authors investigate the nature of an interaction among a suite of traits in each species. It’s not hard to think of a host having a fortress of defenses against attack from a parasite with an arsenal loaded with many weapons.

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