Ploidy and the evolution of parasitism

Abstract

Levels of parasitism are continuously distributed in nature. Models of host-parasite coevolution, however, typically assume that species can be easily characterized as either parasitic or non-parasitic. Consequently, it is poorly understood which factors influence the evolution of parasitism itself. We investigate how ploidy level and the genetic mechanisms underlying infection influence evolution along the continuum of parasitism levels. In order for parasitism to evolve, selective benefits to the successful invasion of hosts must outweigh the losses when encountering resistant hosts. However, we find that exactly where this threshold occurs depends not only on the strength of selection, but also on the genetic model of interaction, the ploidy level in each species, and the nature of the costs to virulence and resistance. With computer simulations, we are able to incorporate more realistic dynamics at the loci underlying species interactions and to extend our analyses in a number of directions, including finite population sizes, multiple alleles and different generation times.

Host-parasite evolution in male-haploid hosts: an individual based network model

“…5). A result similar to those from previous studies (King et al 2012), and in support of the invasion scenarios of M'Gonigle and Otto (2011). The results here being attributable to the proportion of I-S edges, and the general density of edges in the network.…”

“…In general ploidy has been ignored as model factors (Agrawal and Lively 2002;Nuismer and Otto 2004;Otto and Nuismer 2004;Lively 1999, 2007;Schmid-Hempel and Jokela 2002). Those studies that compared the ploidy of hosts on the RQH are few and far between M'Gonigle and Otto 2011;Kidner and Moritz 2013) with only Nuismer and Otto (2004) considering ploidy amoung parasites. Nevertheless, the predictions made for the host species amoung these studies (with different model designs) remain remarkably consistent.…”

“…Most studies make the 'single challenge' assumption: Every host individual is considered to be 'challenged' by a single parasite (Agrawal and Lively 2002;Agrawal 2009;Hodgeson and Otto 2012;M'Gonigle and Otto 2011;Peters and Lively 2007). The single challenge assumption disregards both experimental and theoretical studies on parasites/pathogens.…”

Mutational effects depend on ploidy level: all else is not equal

“…That some mutations have different effects in haploid and homozygous diploid backgrounds is an important result, as theoretical studies often assume that all else is equal when modelling the effects of ploidy, including models about ploidy evolution [14,15], rates of adaptation [16] and host-parasite interactions [17]. A better understanding about when (and why) mutational parameters differ between individuals of varying ploidy may help explain why one ploidy-level predominates in a group of organisms, a longstanding question in evolutionary biology.…”

The Red Queen Process does not Select for High Recombination Rates in Haplodiploid Hosts

“…Since arthropods are not very well known for adaptive immune systems the MAM was adopted as the interaction model over the IMA and GfG models (Wilfert, Gadau and Schmid-Hempel 2007a). However, since the results of previous studies Oswald and Nuismer 2007;M'Gonigle and Otto 2011) suggest the possibility of interdependence between these factors, the results here remain specific to the MAM.…”