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1 Supporting Information 2 3 4 Parasite-mediated selection and its effects on host diversity Parasites can exert a number of different types of selection on host populations, leading 5 to either increased or decreased host diversity. Specifically, parasites can increase host diversity 6 via negative frequency dependent selection or disruptive selection; parasites can decrease host 7 diversity via stabilizing selection, directional selection for increased resistance, or directional 8 selection for increased susceptibility (see main body of article; Figure 1). 9 When determining the type of selection experienced by a population, two pieces of 10 information are useful. First, it is important to know whether there are host-parasite genotype 11 interactions, since these are a prerequisite for negative frequency dependent selection. Studies 12 looking for such interactions usually expose a range of host genotypes to a range of parasite 13 genotypes, and test for significant host genotype x parasite genotype interactions (e.g., Carius, 14 Little & Ebert 2001, Salvaudon, Heraudet & Shykoff 2007). Second, changes in the distribution 15 of susceptibilities (that is, how easy it is to infect a genotype) in the host population should be 16 measured. In many cases, these changes are measured as changes in mean and/or variance (e.g., 17 Brockhurst et al. 2003, Duncan, Mitchell & Little 2006), but the overall distributions of 18 susceptibilities can be compared as well (e.g., Duffy et al. 2008). 19 When measuring changes in the distribution of susceptibilities, a key question is what 20 parasite genotypes to use when assaying susceptibilities. Frequently, a mixture of different 21 parasite genotypes are used (e.g., Brunet & Mundt 2000, Herzog, Müller & Vorburger 2007). In 22 general, the parasite genotypes used should be as representative as possible of those causing the 23 selection. 1 24 It is interesting to note that many studies, and particularly those looking for negative 25 frequency dependent selection, use a third approach as well – mathematical models 26 parameterized for the specific study system (e.g., Decaestecker et al. 2007, Dybdahl & Lively 27 1998). This suggests that combining empirical and theoretical approaches may be a particularly 28 powerful way to study the effects of parasites on host populations. 29 It is also possible to test for parasite-driven evolution using the Lande-Arnold selection 30 gradient method (Lande & Arnold 1983), though this approach is less common. One study used 31 this approach to look for selection on two species of cactus, Echinopsis chilensis and Eulychnia 32 acida driven by a parasitic mistletoe, Tristerix aphyllus (Medel 2000). In this case, there was 33 only weak or no selection on a trait hypothesized to be important to resistance (spine length). 34 This method is quite powerful for detecting directional, stabilizing and disruptive selection; 35 however, it requires the ability to measure both the phenotype and fitness of individuals in the 36 field (Lande & Arnold 1983), making it difficult to apply to many organisms. 37 In Figure 1, we show expectations for the patterns of susceptibility as measured in natural 38 populations. We present the case for a disease with epidemic dynamics because there is a clear 39 period during which selection occurs. Much of the theory, however, considers parasites that are 40 endemic. We expect the qualitative changes in the population to be the same for endemic vs. 41 epidemic diseases, though this is an area worthy of further exploration. 42 In most cases in Figure 1, we assume that the population has an approximately normal 43 distribution of susceptibilities prior to an epidemic, though this will not necessarily be the case. 44 However, for negative frequency dependent selection, a normal “pre-epidemic” distribution is 45 not expected. Rather, the most common genotypes should be the most susceptible, since the 46 parasites best at infecting those genotypes should be the most common (Bell 1982, Hamilton 2 47 1980, Jaenike 1978). Therefore, in the case of negative frequency dependent selection, the pre- 48 epidemic distribution should be skewed so that the highly susceptible genotypes are also the 49 most common. 50 3 51 52 Uses of the term “frequency dependent” While the theoretical literature has clearly shown that parasites can exert different types 53 of selection on their host populations, many empiricists remain unaware of several of the 54 possibilities (most notably the possibility of parasite-mediated disruptive selection). We suspect 55 that the dominant reason for this is simply that some of the possibilities (such as disruptive 56 selection and selection for increased susceptibility) are initially counterintuitive, at least if trade- 57 offs are not explicitly considered. However, another factor that is likely contributing to the 58 confusion is the different uses of the term “frequency dependent” in the host-parasite literature. 59 In this regard, the host-parasite literature mirrors the broader literature, where frequency 60 dependent is used to refer to very different mechanisms (Heino, Metz & Kaitala 1998). This 61 potential confusion is important in the context of the present review, since the nature of 62 transmission can affect evolutionary outcomes (see below). 63 In general, the term “frequency dependent” is used more broadly in the theoretical 64 literature than in the empirical literature (where it is generally used in reference to negative 65 frequency dependent selection). In its broadest sense, frequency dependent selection refers to 66 the idea that the fitness of a genotype depends on the other genotypes present in the population 67 (Futuyma 1998), which is generally true in host-parasite interactions. This can be best 68 understood in light of disease thresholds, which arise because a certain fraction of individuals 69 must be susceptible to a disease in order for the disease to invade that population (that is, in order 70 to be above the disease threshold; Anderson & May 1991, Keeling & Rohani 2008). For 71 example, if a population is dominated by highly resistant phenotypes (and, therefore, is below 72 the disease threshold), the fitness of a highly susceptible phenotype is likely to be higher than in 73 a population dominated by susceptible phenotypes (where the parasite is able to persist and 4 74 attack our focal phenotype). In this case, then, the fitness of a phenotype depends on the other 75 phenotypes in the population, not because those other phenotypes determine the parasite strain 76 that dominates the population (as with negative frequency dependent selection), but because 77 those phenotypes help determine whether the parasite is present in the population at all. It is in 78 this sense that the term "frequency dependence" is generally used in the theoretical host-parasite 79 literature, including in the adaptive dynamics literature (Waxman & Gavrilets 2005). 80 As discussed in the main body of this article, negative frequency dependent selection can 81 arise when there are host-parasite genotype interactions – that is, when the susceptibility of a 82 particular host genotype depends on the parasite genotype to which it is exposed. In this case, 83 parasites "track" the common host genotypes, which reduces the fitness of those common 84 genotypes and favors rare genotypes (Woolhouse et al. 2002). As a result, the fitness of a 85 genotype decreases as its frequency increases, because the parasites that are best at infecting that 86 host genotype become common. When empiricists discuss “frequency dependent selection”, it 87 generally is in reference this more specific case of negative frequency dependent selection. 88 Finally, "frequency dependent” is also used in the host-parasite literature when describing 89 disease transmission (Begon et al. 2002, de Jong, Diekmann & Heesterbeek 1995, Grassly & 90 Fraser 2008). Generally, two transmission terms are considered: density dependent transmission 91 and frequency dependent transmission (Keeling & Rohani 2008). With density dependent 92 transmission, transmission is assumed to scale with the density of hosts; that is, the rate of 93 increase of infected hosts is described by βSI, where β is transmission rate, S is the density of 94 susceptible (that is, uninfected) hosts, and I is the density of infected hosts. In contrast, with 95 frequency dependent transmission, the rate of increase of infected hosts is assumed to scale with 96 the frequency of infected hosts: BSI/N, where N is the density of the host population. Frequency 5 97 dependent transmission is considered particularly common for sexually-transmitted diseases 98 (Anderson & May 1991, May & Anderson 1979), but has also been found in diseases that are not 99 sexually transmitted (e.g., measles in humans: Bjørnstad, Finkenstädt & Grenfell 2002; cowpox 100 in voles and mice: Begon et al. 1999). Whether disease transmission is density dependent or 101 frequency dependent can affect the evolution of host resistance (Antonovics & Thrall 1994). 102 Specifically, Antonovics and Thrall found that directional selection for increased resistance was 103 more likely with density dependent transmission, whereas disruptive selection (leading to 104 coexistence of resistance and susceptible genotypes) was more likely with frequency dependent 105 transmission. 106 107 References 108 Anderson, R. M. & May, R. M. (1991) Infectious diseases of humans: dynamics and control, 109 110 Oxford University Press, Oxford. Antonovics, J. & Thrall, P. H. (1994) The cost of resistance and the maintenance of genetic 111 polymorphism in host-pathogen systems. Proceedings of the Royal Society of London 112 Series B-Biological Sciences, 257, 105-110. 113 Begon, M., Bennett, M., Bowers, R. G., French, N. P., Hazel, S. M. & Turner, J. 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