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GENETIC VARIATION IN RESISTANCE AND FECUNDITY TOLERANCE IN A NATURAL HOST–PATHOGEN INTERACTION
Author(s) -
Parker Benjamin J.,
Garcia Justine R.,
Gerardo Nicole M.
Publication year - 2014
Publication title -
evolution
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.84
H-Index - 199
eISSN - 1558-5646
pISSN - 0014-3820
DOI - 10.1111/evo.12418
Subject(s) - biology , acyrthosiphon pisum , aphid , pathogen , host (biology) , fecundity , coevolution , natural selection , genetic variation , resistance (ecology) , defence mechanisms , zoology , aphididae , genetics , ecology , botany , selection (genetic algorithm) , homoptera , population , pest analysis , gene , demography , artificial intelligence , sociology , computer science
Individuals vary in their ability to defend against pathogens. Determining how natural selection maintains this variation is often difficult, in part because there are multiple ways that organisms defend themselves against pathogens. One important distinction is between mechanisms of resistance that fight off infection, and mechanisms of tolerance that limit the impact of infection on host fitness without influencing pathogen growth. Theory predicts variation among genotypes in resistance, but not necessarily in tolerance. Here, we study variation among pea aphid ( Acyrthosiphon pisum ) genotypes in defense against the fungal pathogen Pandora neoaphidis . It has been well established that pea aphids can harbor symbiotic bacteria that protect them from fungal pathogens. However, it is unclear whether aphid genotypes vary in defense against Pandora in the absence of protective symbionts. We therefore measured resistance and tolerance to fungal infection in aphid lines collected without symbionts, and found variation among lines in survival and in the percent of individuals that formed a sporulating cadaver. We also found evidence of variation in tolerance to the effects of pathogen infection on host fecundity, but no variation in tolerance of pathogen‐induced mortality. We discuss these findings in light of theoretical predictions about host‐pathogen coevolution.