Have you thought that not all the genes in your body might have the same evolutionary interests? The mouse Y chromosome has just been revealed after years of superhuman slog and turns out to be strikingly different from other non-recombining sex chromosomes in two main ways. Firstly, the mouse Y contains almost no DNA signatures of its past as a non sex chromosome. Secondly, most of it isn’t “junk”. Both these observations have shown just how much conflict within a genome can shape the evolution of entire chromosomes.
This post is a guest contribution by Dr. Levi Morran, NIH postdoctoral fellow at Indiana University. Levi studies the role that both coevolutionary relationships and mating systems play in shaping evolutionary trajectories. His research using experimental coevolution to test the Red Queen hypothesis recently appeared in Science and was featured on NPR and the BBC.
I’ll begin by acknowledging that the title of this entry is probably a bit more dramatic than it needs to be. Nonetheless it’s pretty catchy isn’t it?
Given that the human population seems to have survived that whole 2012 Mayan calendar thing without incident, I know several of my friends (I won’t name names, but you know I love you) that would immediately think about zombies upon reading this title. However, I am not particularly concerned about the extinction of the human race at the hands of zombies. For one thing, I need more evidence (or in fact any evidence whatsoever) before I buy the whole “zombies will rise up and end us all” fear. Further, Max Brooks (son of Mel Brooks) has given us a hilarious and potentially mildly effective guide to surviving the zombie apocalypse. Ultimately I am far more concerned about bacteria. To avoid inducing mass panic, I’m not talking about a terrified level of concern here, but certainly concerned enough to give it some thought.
Why bacteria? Well, the human population is currently in an evolutionary arms race with many of the bacterial species that infect us. We continue to hurl scores of antibiotics at bacterial infections, imposing very strong natural selection, with little regard for the evolution of antibiotic resistance in those bacterial populations. Using current strategies in medicine, we are forced to administer greater doses of drugs or develop novel antibiotics to combat infections as the bacteria evolve greater levels of resistance (Levy and Marshall 2004, Martinez et al. 2007). This is a vicious cycle. I believe it is time to develop new strategies of managing our pathogens and treating infections. Thankfully there are many people that agree and are conducting ground-breaking research in this area, like Andrew Read’s group at Penn State University.
A paper by Quan-Guo Zhang and Angus Buckling (2012) takes an experimental evolution approach to begin addressing this issue empirically. In search of a different strategy for curbing the evolution of antibiotic resistance in their experimental populations of the bacterial species Pseudomons flourences, Zhang and Buckling treated their bacterial populations with either antibiotics, a bacteriophage or “phage” (a virus that attacks bacteria), or a combination of the antibiotic and phage. Zhang and Buckling predicted that the combination treatment might be more effective than either antibiotics or phage alone because the combination treatments should better reduce bacterial population sizes and limit their response to selection (Alisky et al. 1998, Chanishvili 2001, Comeau 2007). Additionally, bacterial mutations that confer resistance to antibiotics generally do not also confer resistance to phage, so evolution of resistance to the combination treatments would likely require at least two mutations, and thus require more time to evolve resistance than the other treatments (Chanishvili 2001, Kutateladze 2010). Continue reading
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 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.
Conventional 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.
A paper by Morris and colleagues (2012) has generated some stir among biologists. The authors are proposing the Black Queen hypothesis to explain genomic reductions among free living interacting microbes. Rather than rehash arguments that have been made more eloquently, I’d like to just point out some informative ones
Quick summary over at the New Scientist
In depth critique by Robert T. Gonzalez
What happens when two parasites infect the same host individual? Is the outcome similar to the Thunderdome: two parasites enter, one parasite leaves? Host-parasite interactions are rarely so simple. While a reductionist approach to understanding the interaction of a parasite or pathogen with its host may decompose the system to a single infection, nature is full of much more complex puzzles. Within the host, the battle itself raging between parasites (within-host competition) may have cascading effects on the host.
A recent paper on virulence caught my eye (Bashey et al., 2012) which provides an update to a very interesting result from the group a few years ago. The system includes bacterial parasites, along with parasitic nematodes, that infect insect larvae and eat/digest them from the inside out. Vigneux et al. (2008) found that when multiple parasite isolates are mixed in a host, the host mortality decreased. However, this only occurred when the isolates were not related. In the experiment, the researchers created low relatedness by mixing populations with migration. I reviewed the 2008 paper over at the Coevolvers blog, my personal science blog. The hypothesis was that chemical warfare among the parasites decreased the parasite load and reduced the negative effects on the host, virulence.
What are the evolutionary consequences of parasite superinfection (i.e. simultaneous infection by multiple parasites)? When parasites are genetically distinct, coexistence within a host generates conflict because of limited resources. How this conflict is resolved is the source of evolutionary research on the evolution of parasite life history traits such as virulence, the negative effects on the host caused by infection, and transmission mode, how parasites infect a new host. The transmission mode of a parasite is often characterized as occurring in one of two different modes: vertical or horizontal. With vertical transmission, an offspring obtains its parasites directly from its parents. In contrast, with horizontal transmission, infections occur either directly from the environment or contagiously by infection from other individuals.
My interest in the evolution of transmission mode in parasites and symbionts led me to a recent paper (Ben-Ami et al. 2011), which addresses the consequences of superinfection by two different parasites with different transmission modes of the waterflea, Daphnia magna, on virulence and parasite fecundity. Pasteuria ramosa is a castrating, horizontally transmitted, blood-infecting bacterium where spores are produced from the cadaver of the host Daphnia. Octosporea bayeri, a microsporidium, utilizes both vertical transmission to eggs and horizontal transmission via waterborne spores.