Host-parasite system in microbial life

Genetics of Adaptation Graduate Seminar
Author: AA


Plants and their pollinators, predator and prey, host and parasite, and viruses and the organisms they live in are only several examples of coevolutionary associations: over time, the interactions between organisms can result in mutual adaptations during their evolution. But how can they coevolve, and what does coevolution mean?


According to one of the first definitions, coevolution is "the change of a biological object triggered by the change of a related object" (Futuyma & Slatkin, 1983). Coevolution can occur at different levels of the life of an organization; it can be biochemical processes, changes in cell structure and shape, behavioral responses, or even changes in population sizes.  Coevolutionary processes are often complicated and involve both genetic mechanisms and morphological/behaviorial adaptations.

             
Host-parasite system is a good model to study coevolution. There are many “popular” host-parasite interactions that are studied very well: mammals and tapeworms, snails and flatworms, human and bacteria, human and insects and so on. Some parasites can use only one host (tightly specific) and these organisms, therefore, evolve together (or co-evolve). Other parasites can develop in a variety of hosts (universally adapted).


Evolutionary studies on host-parasite interactions often focus on two sides of this system: the defensive mechanisms of hosts, and the potential for adaptation of the parasites. Authors of the paper “The effect of migration on local adaptation in a coevolving host–parasite system” (Morgan et al. 2005, Nature) considered the latter.


Parasite adaptation is a controversial topic; there are studies that support the local adaptation of parasites to their hosts, and studies that report no evidence of parasite adaptation.


However, this study is somewhat unique in that the host was bacteria, an organism that we generally think more often as the parasite rather than the host. The authors had good reason for choosing this model, as its use allowed for (1) a large population size, (2) short generation times, and (3) an antagonistic nature of the interaction with the parasite. All those things, according to the authors, were favorable for evolution.           


Specifically, the researchers used the bacteria Pseudomonas fluorescens (Fig. 1) as the host, and the bacteriophage (lytic DNA phage SBW25f2) as the parasite. The members of the Pseudomonas genus are widespread in nature, inhabiting soil, water, plants, and animals (including humans). Most of them are pathogens. For example, Pseudomonas syringae can act as plant pathogen; whereas Pseudomonas aeruginosa is the most common human pathogen which can cause nosocomial infections such as pneumonia, urinary tract infections, and bacteremia (= the presence of bacteria in the blood).

Fig.1. Pseudomonas. Source

Fig. 2. Bacteriophage (on the left, Source) and bacteriophages attached to a bacterial cell (on the right, Source).

A bacteriophage (“phage” means “to eat” from Greek) is one of a number of viruses that infect bacteria (Fig.2). Phages are widely distributed and can be found in all reservoirs populated by bacterial hosts, such as soil or the intestines of animals. Sea water is one of the densest natural sources for phages; there are up to 9×10⁸ phages per milliliter and up to 70% of marine bacteria may be infected by phages (Wommack and Colwell,  2000).


Although we already know that host and parasite behavior are very important for this interaction, we don’t understand the impact of host and parasite migration, that seems to have no primary effect on the adaptation of any organism. Nevertheless, migration between populations is very important in terms of genetic variation; beneficial genes can be introduced from one population to another. Many experimental studies have demonstrated the role of migration in coevolutionary processes. However,  whether migration rates of hosts or parasites have an effect on their local adaptation, remains poorly investigated. The authors’ prediction was that parasites were locally adapted if they migrated more than their hosts, whereas hosts were locally adapted if they migrated more than their parasites.


The experimental design of this work was impressive. The main idea was to grow the necessary amount of bacteria populations and particles of phages (“particle” – because they act as viruses), and then, to perform several cultures with different ratios of migration either bacteria, or phage. The authors cultured 6 populations with 10 ⁸ cells of bacteria (that is approximately the population of both North and Latin America) and 10⁵  particles of phage, and perform 5 treatments: control; 10% bacteria migration, 0% phage migration; 0.1% bacteria migration, 0% phage migration; 0% bacteria migration, 10% phage migration; and 0% bacteria migration, 0.1% phage migration. Author performed the migration as the removal of a certain amount of either bacteria, or phage from the culture.


After allowing for migration, the authors measured the local adaptation of host and parasite—they assayed this as either resistance on the part of the bacteria, or conversely the ability of the phage to infect the bacteria. In practice, it looked like any visible inhibition of bacterial growth when exposed to the phage.

And here are the results:

Figure 3. Mean local adaptation of parasites. Data are averaged over six populations and six time points for different migration treatments. Results are means ± s.e.m. across populations. P, phage migration; B, bacterial migration (Morgan et al., 2005).

The results of the experiments in this paper confirmed, once again, that the local adaptation of parasites exists, and that the migration has an effect on this adaptation. What they found was that phage migration increased phage local adaptation, whereas bacterial migration had little effect.


They also observed that the effect of migration was asymmetric: parasite migration increased parasite local adaptation relative to unmigrated populations; whereas host migration did not decrease parasite adaptation (its migration just had no any effect on parasites). The authors explained that by the following: “parasites are locally maladapted in the absence of any migration, and host migration is unable to increase parasite local maladaptation any further”.


These results might have important implications. Since the authors demonstrated that parasite migration could result in parasite local adaptation through their evolutionary advantage in a host-parasite coevolution, it can be addressed to global interactions, for examples, in human-parasite system. Parasites have inhabited humans since the beginning of life; their interactions may increase both parasite transmission and their infectivity to their local hosts, and therefore, that might facilitate the development and spreading of human diseases.


References:

Morgan, A. D., S. Gandon, et al. (2005). "The effect of migration on local adaptation in a coevolving host–parasite system." Nature 437(7056): 253-256.

Futuyma, D. J. and M. Slatkin (editors). (1983). “Coevolution”. Sunderland, Massachusetts: Sinauer Associates,555 pp.

Wommack, K. E.; Colwell, R. R. (2000). “Viroplankton: viruses in auquatic ecosystems”. Microbiology and Molecular Biology Reviews 64 (1): 69.