Thermal plasticity in Drosophila melanogaster populations from eastern Australia: quantitative traits to transcripts.

The flexibility afforded to genotypes in different environments by phenotypic plasticity is of interest to biologists studying thermal adaptation because of the thermal lability of many traits. Differences in thermal performance and reaction norms can provide insight into the evolution of thermal adaptation to explore broader questions such as species distributions and persistence under climate change. One approach is to study the effects of temperature on fitness, morphological and more recently gene expression traits in populations from different climatic origins. The diverse climatic conditions experienced by Drosophila melanogaster along the eastern Australian temperate-tropical gradient are ideal given the high degree of continuous trait differentiation, but reaction norm variation has not been well studied in this system. Here, we reared a tropical and temperate population from the ends of the gradient over six developmental temperatures and examined reaction norm variation for five quantitative traits including thermal performance for fecundity, and reaction norms for thermotolerance, body size, viability and 23 transcript-level traits. Despite genetic variation for some quantitative traits, we found no differentiation between the populations for fecundity thermal optima and breadth, and the reaction norms for the other traits were largely parallel, supporting previous work suggesting that thermal evolution occurs by changes in trait means rather than by reaction norm shifts. We examined reaction norm variation in our expanded thermal regime for a gene set shown to previously exhibit GxE for expression plasticity in east Australian flies, as well as key heat-shock genes. Although there were differences in curvature between the populations suggesting a higher degree of thermal plasticity in expression patterns than for the quantitative traits, we found little evidence to support a role for genetic variation in maintaining expression plasticity.

The effects of plasma cortisol elevation on total and differential leukocyte counts in response to heavy-resistance exercise.

The purpose of this study was to examine the impact of heavy-resistance exercise-induced elevations of plasma cortisol on circulating leukocyte counts. Nine healthy, recreationally weight-trained men volunteered for this investigation. Two exercise protocols were employed. Protocol 1 (P-1) consisted of eight sets of ten-repetition maximum leg-press exercise with 1-min rest periods between sets. Protocol 2 (P-2) was identical except for 3-min rest periods. A non-exercise protocol was used as a control treatment (C). Venous blood samples, heart rates and ratings of perceived exertion were obtained pre-, mid- and 5 min post-exercise. In order to examine the maximal influence of cortisol on leukocyte counts, we placed the subject's highest magnitude of cortisol change in response to one of the heavy-resistance exercise protocols in what we designated as the response protocol (R) and the other value was placed into what was designated as the non-response protocol (NR) for analysis. Significant increases in cortisol occurred from pre- to post-exercise for P-1 [mean (SD) 241.4 (25.0) to 302.0 (60.0)nmol . 1(-1)] and in the R conditions pre- to mid- and pre- to post-exercise [218.0(0.0) to 302.4 (37.1) to 326.8 (51.9)nmol . 1(-1)]. No significant changes in cortisol occurred for P-2, NR or the control conditions. Significant increases in total leukocyte counts occurred from pre- to mid- and pre- to post-exercise both for R [5.6 (0.4) to 7.4 (0.3) to 7.3 (0.3) cells . 10(9) . 1(-1)] and NR [5.7 (0.3) to 6.9 (0.4) to 7.1(0.4) cells . 10(9) . l(-1)]. No significant changes in differential leukocyte counts occurred. In addition, no significant correlations between cortisol and total or differential leukocyte counts were observed. These data indicate that acute increases in total leukocytes along with no changes in differential leukocyte counts can occur in response to heavy-resistance exercise that does not significantly elevate plasma cortisol concentrations.