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Host-parasite coevolution promotes innovation through deformations in fitness landscapes.

ABSTRACT: During the struggle for survival, populations occasionally evolve new functions that give them access to untapped ecological opportunities. Theory suggests that coevolution between species can promote the evolution of such innovations by deforming fitness landscapes in ways that open new adaptive pathways. We directly tested this idea by using high-throughput gene editing-phenotyping technology (MAGE-Seq) to measure the fitness landscape of a virus, bacteriophage λ, as it coevolved with its host, the bacterium Escherichia coli. An analysis of the empirical fitness landscape revealed mutation-by-mutation-by-host-genotype interactions that demonstrate coevolution modified the contours of λ's landscape. Computer simulations of λ's evolution on a static versus shifting fitness landscape showed that the changes in contours increased λ's chances of evolving the ability to use a new host receptor. By coupling sequencing and pairwise competition experiments, we demonstrated that the first mutation λ evolved en route to the innovation would only evolve in the presence of the ancestral host, whereas later steps in λ's evolution required the shift to a resistant host. When time-shift replays of the coevolution experiment were run where host evolution was artificially accelerated, λ did not innovate to use the new receptor. This study provides direct evidence for the role of coevolution in driving evolutionary novelty and provides a quantitative framework for predicting evolution in coevolving ecological communities.

SUBMITTER: Gupta A

PROVIDER: S-EPMC9259030 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Population mixing promotes arms race host-parasite coevolution.

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Project description:Host-parasite coevolution can influence interactions of the host and parasite with the wider ecological community. One way that this may manifest is in cross-resistance towards other parasites, which has been observed to occur in some host-parasite evolution experiments. In this paper, we test for cross-resistance towards Bacillus thuringiensis and Pseudomonasentomophila in the red flour beetle Triboliumcastaneum, which was previously allowed to coevolve with the generalist entomopathogenic fungus Beauveriabassiana. We combine survival and gene expression assays upon infection to test for cross-resistance and underlying mechanisms. We show that larvae of T.castaneum that evolved with B.bassiana under coevolutionary conditions were positively cross-resistant to the bacterium B. thuringiensis, but not P.entomophila. Positive cross-resistance was mirrored at the gene expression level with markers that were representative of the oral route of infection being upregulated upon B.bassiana exposure. We find that positive cross-resistance towards B. thuringiensis evolved in T.castaneum as a consequence of its coevolutionary interactions with B.bassiana. This cross-resistance appears to be a consequence of resistance to oral toxicity. The fact that coevolution with B.bassiana results in resistance to B. thuringiensis, but not P.entomophila implies that B. thuringiensis and B.bassiana may share mechanisms of infection or toxicity not shared by P.entomophila. This supports previous suggestions that B.bassiana may possess Cry-like toxins, similar to those found in B. thuringiensis, which allow it to infect orally.

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Project description:Understanding how parasites adapt to changes in host resistance is crucial to evolutionary epidemiology. Experimental studies have demonstrated that parasites are more capable of adapting to gradual, rather than sudden changes in host phenotype, as the latter may require multiple mutations that are unlikely to arise simultaneously. A key, but as yet unexplored factor is precisely how interactions between mutations (epistasis) affect parasite evolution. Here, we investigate this phenomenon in the context of infectivity range, where parasites may experience selection to infect broader sets of genotypes. When epistasis is strongly positive, we find that parasites are unlikely to evolve broader infectivity ranges if hosts exhibit sudden, rather than gradual changes in phenotype, in close agreement with empirical observations. This is due to a low probability of fixing multiple mutations that individually confer no immediate advantage. When epistasis is weaker, parasites are more likely to evolve broader infectivity ranges if hosts make sudden changes in phenotype, which can be explained by a balance between mutation supply and selection. Thus, we demonstrate that both the rate of phenotypic change in hosts and the form of epistasis between mutations in parasites are crucial in shaping the evolution of infectivity range.

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