Abstract
Twelve replicate populations of Drosophila melanogaster, all derived from a common ancestor, were independently evolved for 34+ generations in one of three treatment environments of varying PO2: hypoxia (5.0–10.1 kPa), normoxia (21.3 kPa), and hyperoxia (40.5 kPa). Several traits related to whole animal performance and metabolism were assayed at various stages via “common garden” and reciprocal transplant assays to directly compare evolved and acclimatory differences among treatments. Results clearly demonstrate the evolution of a greater tolerance to acute hypoxia in the hypoxia-evolved populations, consistent with adaptation to this environment. Greater hypoxia tolerance was associated with an increase in citrate synthase activity in fly homogenate when compared to normoxic (control) populations, suggesting an increase in mitochondrial volume density in these populations. In contrast, no direct evidence of increased performance of the hyperoxia-evolved populations was detected, although a significant decrease in the tolerance of these populations to acute hypoxia suggests a cost to adaptation to hyperoxia. Hyperoxia-evolved populations had lower productivity overall (i.e., across treatment environments) and there was no evidence that hypoxia or hyperoxia-evolved populations had greatest productivity or longevity in their respective treatment environments, suggesting that these assays failed to capture the components of fitness relevant to adaptation.
Highlights
Deviation from normal atmospheric partial pressure of O2 imposes biological consequences in many aerobic organisms
Studies examining the effects of hyperoxia have focused on the extent and location of oxidative damage resulting from high aPO2 environments, behaviours associated with preventing such damage, as well as the consequences of oxidative damage to mitochondrial physiology/phenotype [6,12,13]
Post-hoc analyses revealed that all three treatments differed significantly from one another within each generation, with hypoxia-evolved flies being more tolerant than the normoxiaevolved flies which were more tolerant than the hyperoxia-evolved flies (Fig. 1)
Summary
Deviation from normal atmospheric partial pressure of O2 (normoxia: aPO2) imposes biological consequences in many aerobic organisms. Under hypoxic conditions, where aPO2 is reduced, aerobic metabolism is impacted and several acclimatory processes can be triggered at many levels of organization ranging from increased O2 uptake [1,2] to changes in mitochondrial physiology/metabolism [3]. Previous work examining the effects of altered aPO2 on insects has tended to focus, not exclusively, on hypoxia and its consequences for a variety of traits, addressing phenotypic plasticity, respiratory physiology, and aerobic/anaerobic metabolism, as well as evolved responses to artificial selection for increased hypoxia tolerance [3,7,8,9,10,11]. Studies examining the effects of hyperoxia have focused on the extent and location of oxidative damage resulting from high aPO2 environments, behaviours associated with preventing such damage, as well as the consequences of oxidative damage to mitochondrial physiology/phenotype [6,12,13]. Studies have examined if evolved responses differed from acclimatory responses with respect to respiratory physiology and longevity [14,15]
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