Premium
Comparing population response to contaminants between laboratory and field: an approach using Daphnia magna ephippial egg banks
Author(s) -
Barata C.,
Baird D. J.,
Amat F.,
Soares A. M. V. M.
Publication year - 2000
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 - 10.1046/j.1365-2435.2000.00445.x
Subject(s) - biology , toxicant , daphnia magna , population , phenotypic plasticity , zoology , ecology , avian clutch size , fecundity , toxicology , reproduction , toxicity , demography , chemistry , organic chemistry , sociology
Abstract 1. The life‐history responses of one field and two laboratory populations of Daphnia magna were studied under exposure to cadmium and ethyl parathion to assess by how much the response to toxic chemicals of laboratory populations with low genetic diversity differs from the response of genetically diverse field populations. 2. The field population was represented by at least 50 unique clones hatched from resting eggs (ephippia) collected at the beginning of the growing season from a temporary water‐body located in the north‐east Mediterranean Spanish coast. The laboratory populations were clonal lines established from two geographically and genetically distinct genotypes, which differed in their tolerance to cadmium and ethyl parathion. Toxicant effects on the mean and the variance of life‐history responses of the laboratory and the field populations were determined. For the field population, toxicant effects on the components of variance of primary fitness traits were also studied. 3. In addition to lethal effects, exposure to cadmium had strong sub‐lethal effects on clutch size and age at first reproduction whereas ethyl parathion only affected juvenile survival. The results reported for life‐history responses showed that the field population had a similar or greater mean tolerance to cadmium and ethyl parathion than the laboratory populations, but the breadth of its tolerance distribution (measured as the coefficient of variation, CV) was higher. Furthermore in contrast with the field population, laboratory populations did not show increased phenotypic plasticity (measured as CV) under increasing toxicant exposure. A further analysis of the components of variability for life‐history responses of the field population showed that increases in phenotypic plasticity with exposure levels were explained by increased levels of genetic variability. 4. These results support the conclusion that as the tolerance of a field population is strongly influenced by genetic factors, the use of genetically homogeneous laboratory populations has limited relevance in predicting long‐term responses of field populations to toxic chemicals. However, this conclusion must remain tentative until further supporting evidence is obtained from this and other species.