Acclimation and adaptation to common marine pollutants in the copepod Tigriopus californicus.

Establishing water quality criteria using bioassays is complicated by variation in chemical tolerance between populations. Two major contributors to this variation are acclimation and adaptation, which are both linked to exposure history, but differ in how long their effects are maintained. Our study examines how tolerance changes over multiple generations of exposure to two common marine pollutants, copper (Cu) and tributyltin oxide (TBTO), in a sexually reproducing marine copepod, Tigriopus californicus. Lines of T. californicus were chronically exposed to sub-lethal levels of Cu and TBTO for 12 generations followed by a recovery period of 3 generations in seawater control conditions. At each generation, the average number of offspring produced and survived to 28 d was determined and used as the metric of tolerance. Lines exposed to Cu and TBTO showed an overall increase in tolerance over time. Increased Cu tolerance arose by generation 3 in the chronically exposed lines and was lost after 3 generations in seawater control conditions. Increased TBTO tolerance was detected at generation 7 and was maintained even after 3 generations in seawater control conditions. It was concluded from this study that tolerance to Cu is consistent with acclimation, a quick gain and loss of tolerance. In contrast, TBTO tolerance is consistent with adaptation, in which onset of tolerance was delayed relative to an acclimation response and maintained in the absence of exposure. These findings illustrate that consideration of exposure history is necessary when using bioassays to measure chemical tolerance.

Constant light-induced retinal damage and the RPE65-MET450 variant: assessment of the NZW/LacJ mouse.

PURPOSE: In a previous constant light-induced retinal damage (CLD) quantitative genetics study between the albino C57BL/6J-c2J (B6al) and BALB/c mouse strains, we identified a very strong and highly significant quantitative trait locus (QTL) on distal Chr 3 that we associated with a variant of the Rpe65 gene. The B6al strain carries the MET450 variant of RPE65 and is resistant to CLD while the BALB/c strain carries the LEU450 variant and is sensitive. Since then, we have discovered that the NZW/LacJ (NZW) albino mouse strain is sensitive to CLD but carries the MET450 variant of RPE65. The purpose of this study was to determine if the NZW mouse disproves the hypothesis that the MET450 variant of RPE65 protects the mouse retina against constant light-induced retinal damage. METHODS: F2 progeny were bred from an intercross between the NZW/LacJ and B6al mouse strains. After a prolonged exposure to moderate constant light, F2 mice were phenotyped for retinal outer nuclear layer thickness as the quantitative trait. A subset of 156 of the 201 F2 mice was genotyped for a set of markers spanning the genome, and any marker with a significant association with the quantitative trait was genotyped in the remaining 45 F2s. Data were analyzed for QTL by the Map Manager QTX software. RESULTS: No QTL was identified at distal Chr 3, although several QTL on Chrs 1 (two), 10, 13, 14, 16, and X were detected. One QTL on middle Chr 1 (LOD 5.22) mapped to the same location of a QTL (LOD 6.8) in a previous intense, short exposure light-induced retinal damage study conducted with an intercross between the 129S1/SvImJ and BALB/c strains. QTL on Chrs 1 (distal), 10, and 14 also appeared in other retinal damage quantitative genetics studies. Three pairs of genes exhibited significant epistatic effects. Two of the pairs involved synergistic interactions between NZW and B6al alleles, and the third between two B6al alleles. CONCLUSIONS: If another gene besides Rpe65 was responsible for the QTL in the original BALB/c x B6al study, and the NZW mouse carried a light sensitive allele of this gene, a QTL should have been present in this study. Since a QTL on Chr 3 was not found, the hypothesis that RPE65-MET450 protects the retina from constant light-induced damage is left intact. The explanation for the NZW mouse being sensitive to constant light while carrying the RPE65-MET450 variant is that other light sensitive QTL (gene alleles) negate the protective effect.