MHC class I expression dependent on bacterial infection and parental factors in whitefish embryos (Salmonidae).

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2013

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info:eu-repo/semantics/altIdentifier/doi/10.1111/mec.12457

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info:eu-repo/semantics/altIdentifier/pmid/24028333

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info:eu-repo/semantics/altIdentifier/eissn/1365-294X

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info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_BCE74E386F8B8

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E.S. Clark et al., « MHC class I expression dependent on bacterial infection and parental factors in whitefish embryos (Salmonidae). », Serveur académique Lausannois, ID : 10.1111/mec.12457


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Ecological conditions can influence not only the expression of a phenotype, but also the heritability of a trait. As such, heritable variation for a trait needs to be studied across environments. We have investigated how pathogen challenge affects the expression of MHC genes in embryos of the lake whitefish Coregonus palaea. In order to experimentally separate paternal (i.e. genetic) from maternal and environmental effects, and determine whether and how stress affects the heritable variation for MHC expression, embryos were produced in full-factorial in vitro fertilizations, reared singly, and exposed at 208 degree days (late-eyed stage) to either one of two strains of Pseudomonas fluorescens that differ in their virulence characteristics (one increased mortality, while both delayed hatching time). Gene expression was assessed 48 h postinoculation, and virulence effects of the bacterial infection were monitored until hatching. We found no evidence of MHC class II expression at this stage of development. MHC class I expression was markedly down-regulated in reaction to both pseudomonads. While MHC expression could not be linked to embryo survival, the less the gene was expressed, the earlier the embryos hatched within each treatment group, possibly due to trade-offs between immune function and developmental rate or further factors that affect both hatching timing and MHC expression. We found significant additive genetic variance for MHC class I expression in some treatments. That is, changes in pathogen pressures could induce rapid evolution in MHC class I expression. However, we found no additive genetic variance in reaction norms in our study population.

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