Data from: Indirect genetic effects underlie oxygen-limited thermal tolerance within a coastal population of chinook salmon Muñoz, Nicolas J.; Anttila, Katja; Chen, Zhongqi; Heath, John W.; Farrell, Anthony P.; Neff, Bryan D.; Munoz, N. J.
With global temperatures projected to surpass the limits of thermal tolerance for many species, evaluating the heritable variation underlying thermal tolerance is critical for understanding the potential for adaptation to climate change. We examined the evolutionary potential of thermal tolerance within a population of chinook salmon (Oncorhynchus tshawytscha) by conducting a full-factorial breeding design and measuring the thermal performance of cardiac function and the critical thermal maximum (CTmax) of offspring from each family. Additive genetic variation in offspring phenotype was mostly negligible, although these direct genetic effects explained 53% of the variation in resting heart rate (fH). Conversely, maternal effects had a significant influence on resting fH, scope for fH, cardiac arrhythmia temperature and CTmax. These maternal effects were associated with egg size, as indicated by strong relationships between the mean egg diameter of mothers and offspring thermal tolerance. Because egg size can be highly heritable in chinook salmon, our finding indicates that the maternal effects of egg size constitute an indirect genetic effect contributing to thermal tolerance. Such indirect genetic effects could accelerate evolutionary responses to the selection imposed by rising temperatures and could contribute to the population-specific thermal tolerance that has recently been uncovered among Pacific salmon populations.; Usage notes
Electronic Supplementary Material (data)The heart rate and CTmax data from all individuals used in this study. These data were collected from 25 different families of chinook salmon (5 females and 5 males mated in all combinations). Heart rates were counted from electrocardiograms and recorded along with the corresponding temperature. These data were then analyzed to find the Arrhenius break temperature of heart rate, which corresponds to a drop in the temperature sensitivity (Q10) of heart rate. The additive genetic, non-additive genetic, and maternal effects contributing to cardiac performance and CTmax were calculated by partitioning the variation in these phenotypes to Sire (i.e. father) and Dam (i.e. mother) ID and their interaction using a two-way ANOVA.