Abstracts (first author)

Talk 

Plastic traits of whitefish dependent on the interaction of pathogens, host developmental stage, and genetics

Author(s): Clark ES, Pompini M, Marques da Cunha L, Wedekind C

Summary:

Phenotypic plasticity may evolve in response to environmental changes in populations with sufficient genetic variation for the reaction norms. We used the whitefish Coregonus palaea to experimentally study the interplay of ecology, genetics, and development on the evolutionary potential of plastic traits. In order to disentangle maternal from paternal contributions, and the likely effects of developmental stage from ecological effects, we sampled a natural population, used gametes for full-factorial in vitro fertilizations, raised the resulting offspring singly at controlled conditions, and exposed them at one of several points during development to the opportunistic pathogen, Pseudomonas fluorescens. Inoculation with the bacterium increased embryonic mortality and resulted in delayed hatching of smaller, less developed larvae. Vulnerability to infection increased distinctly over embryo development. This change coincided with a shift in the importance of maternal to additive genetic effects on survival. Timing of exposure also affected whether there was genetic variability for trait plasticity, and whether traits were correlated across environments. Our results demonstrate that additive genetic effects on plastic traits and of trait plasticities critically depend on developmental stage and hence on the timing of a stressful event.



Abstracts (coauthor)

Summary:

One of the most common chemical pollutants is 17α-ethinylestradiol (EE2), a synthetic estrogen used in most contraceptive pills. Compared to other estrogens, EE2 is rather persistent in the environment and often found in concentrations that could be harmful to fish development. We set up an experiment (i) to describe the toxicity of EE2 during early development in the whitefish Coregonus palaea and (ii) to test whether there is additive genetic variance in the tolerance to the pollutant within a natural population. We sampled a natural population of whitefish and collected their gametes for in vitro fertilization. In order to separate paternal (i.e. additive genetic) from maternal environmental effects on embryo and larval development, we used a full-factorial breeding design, raised large numbers of embryos separately in individual containers, and exposed them to various EE2 concentrations (0ng/L, 0.5ng/L, 1ng/L, 10ng/L and 100ng/L). We are currently recording growth, survival, and gonad development. Variance components can very soon be calculated and will give us an idea about the potential of rapid evolution in a common fish in response to a common pollutant.

Summary:

Hatching is an important niche shift, and embryos in a wide range of taxa can either accelerate or delay this life-history switch in order to avoid stage-specific risks. Such behavior can occur in response to stress itself and to chemical cues that allow anticipation of stress. We studied the genetic organization of this phenotypic plasticity and tested whether there are differences among populations and across environments in order to learn more about the evolutionary potential of stress-induced hatching. As a study species, we chose the brown trout (Salmo trutta; Salmonidae). Gametes were collected from five natural populations (within one river network) and used for full-factorial in vitro fertilizations. The resulting embryos were either directly infected with Pseudomonas fluorescens or were exposed to waterborne cues from P. fluorescens-infected conspecifics. We found that direct inoculation with P. fluorescens increased embryonic mortality and induced hatching in all host populations. Exposure to waterborne cues revealed population-specific responses. We found significant additive genetic variation for hatching time, and genetic variation in trait plasticity. In conclusion, hatching is induced in response to infection and can be affected by waterborne cues of infection, but populations and families differ in their reaction to the latter.

Contacts

Chairman: Octávio S. Paulo
Tel: 00 351 217500614 direct
Tel: 00 351 217500000 ext22359
Fax: 00 351 217500028
email: mail@eseb2013.com

Address

XIV Congress of the European Society for Evolutionary Biology

Organization Team
Department of Animal Biology (DBA)
Faculty of Sciences of the University of Lisbon
P-1749-016 Lisbon
Portugal

Website

Computational Biology & Population Genomics Group 
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