Evidence of population genetic effects of long-term exposure to contaminated sediments-a multi-endpoint study with copepods.
In the environment, pollution generally acts over long time scales and exerts exposure of multiple toxicants on the organisms living there. Recent findings show that pollution can alter the genetics of populations. However, few of these studies have focused on long-term exposure of mixtures of substances. The relatively short generation time (ca. 4-5 weeks in sediments) of the harpacticoid copepod Attheyella crassa makes it suitable for multigenerational exposure studies. Here, A. crassa copepods were exposed for 60 and 120 days to naturally contaminated sediments (i.e., Svindersviken and Trosa; each in a concentration series including 50% contaminated sediment mixed with 50% control sediment and 100% contaminated sediment), and for 120 days to control sediment spiked with copper. We assayed changes in F(ST) (fixation index), which indicates if there is any population subdivision (i.e., structure) between the samples, expected heterozygosity, percent polymorphic loci, as well as abundance. There was a significant decrease in total abundance after 60 days in both of the 100% naturally contaminated sediments. This abundance bottleneck recovered in the Trosa treatment after 120 days but not in the Svindersviken treatment. After 120 days, there were fewer males in the 100% naturally contaminated sediments compared to the control, possibly caused by smaller size of males resulting in higher surface: body volume ratio in contact with toxic chemicals. In the copper treatment there was a significant decrease in genetic diversity after 120 days, although abundance remained unchanged. Neither of the naturally contaminated sediments (50 and 100%) affected genetic diversity after 120 days but they all had high within treatment F(ST) values, with highest F(ST) in both 100% treatments. This indicates differentiation between the replicates and seems to be a consequence of multi-toxicant exposure, which likely caused selective mortality against highly sensitive genotypes. We further assayed two growth-related measures, i.e., RNA content and cephalothorax length, but none of these endpoints differed between any of the treatments and the control. In conclusion, the results of the present study support the hypothesis that toxicant exposure can reduce genetic diversity and cause population differentiation. Loss of genetic diversity is of great concern since it implies reduced adaptive potential of populations in the face of future environmental change.
Gardeström
Johanna
J
Department of Systems Ecology, Stockholm University, SE-10691 Stockholm, Sweden. johanna@ecology.su.se
Dahl
Ulrika
U
Kotsalainen
Ola
O
Maxson
Anders
A
Elfwing
Tina
T
Grahn
Mats
M
Bengtsson
Bengt-Erik
BE
Breitholtz
Magnus
M
D054458:Amplified Fragment Length Polymorphism Analysis / Q000662:veterinary; D000818:Animals; D033342:Copepoda / Q000187:drug effects* / Q000254:growth & development; D003300:Copper / Q000633:toxicity*; D004781:Environmental Exposure; D005260:Female; D014644:Genetic Variation / Q000187:drug effects; D019015:Geologic Sediments / Q000032:analysis; D006579:Heterozygote; D008297:Male; D019216:Metals, Heavy / Q000032:analysis; D011156:Population Density; D012313:RNA / Q000032:analysis; D013997:Time Factors; D014874:Water Pollutants, Chemical / Q000633:toxicity*
D019216:Metals, Heavy; D014874:Water Pollutants, Chemical; D012313:RNA; D003300:Copper