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Maternal and paternal contributions to pathogen resistance dependent on development stage in a whitefish ( S almonidae)
Author(s) -
Clark Emily S.,
Pompini Manuel,
Marques da Cunha Lucas,
Wedekind Claus
Publication year - 2014
Publication title -
functional ecology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 154
eISSN - 1365-2435
pISSN - 0269-8463
DOI - 10.1111/1365-2435.12214
Subject(s) - biology , maternal effect , offspring , hatching , coregonus , heritability , additive genetic effects , genetics , population , larva , genetic variation , genotype , embryo , zoology , natural selection , ecology , demography , pregnancy , gene , fishery , sociology , fish <actinopterygii>
Summary It is often assumed that maternal and paternal contributions to offspring phenotype change over the lifetime of an individual. However, studies on parental effects typically suffer from the problems that heritabilities and maternal environmental effects are difficult to separate, and that both may depend on environmental factors and developmental stage. In order to experimentally disentangle maternal from paternal contributions and the likely effects of developmental stage from ecological effects, we sampled a natural population of the whitefish Coregonus palaea, used gametes for full‐factorial in vitro fertilizations, raised over 10 000 of the resulting offspring singly at controlled conditions, and exposed them at different points during embryonic development to one of two strains of Pseudomonas fluorescens that differed in their virulence characteristics (only one caused mortality, while both delayed hatching and reduced growth). Vulnerability to infection increased markedly over embryo development. This change coincided with a distinct shift in the importance of maternal to additive genetic effects on survival. Timing of exposure also affected the variance components for hatching time and larval length, but in a less consistent direction than the variance components for mortality. No significant genetic variation was found for any reaction norms across time points of exposure, indicating a uniformity among genotypes in how susceptibility changed over development. Phenotypes were also typically correlated across time points, which could constrain the evolution of the reaction norms. Our experiment demonstrates that the relative maternal and paternal contributions to susceptibility to an infection, and hence the evolutionary potential to respond to pathogen‐induced selection, depends not only on the kind of pathogenic stress but also on the timing of the challenge.