Hypoxia and the metabolic phenotype of Daphnia
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Environmental hypoxia is a phenomenon in which low oxygen conditions force organisms to respond behaviourally and physiologically to survive in an otherwise lethal habitat. Animals display different mechanisms to cope with the harsh living conditions of a hypoxic environment, most of which can be summarized as: (i) improvement of oxygen transport capacity, (ii) improvement of oxygen storage, and (iii) supply of energy via anaerobic metabolism. Daphnia respond to hypoxia by increasing the expression of extracellular hemoglobin (Hb), an oxygen transport/storage protein. It is generally thought that this upregulation is used as a strategy to sustain sufficient oxygenation to tissues, allowing Daphnia to stay systemically normoxic even when the environment is hypoxic. Although the changes/differences in Hb levels have been studied in many contexts, very little has been done exploring the basic properties of energy metabolism in Daphnia. My focus was on the link between the Hb response and the metabolic phenotype. I sampled different Daphnia species from 20 lakes in the Frontenac Arch Biosphere. The resulting metabolite analyses support the idea that the benefit of Hb is facilitating oxygen delivery rather than to increase oxygen storage. I found a distinct lack of coordination in the responses of the glycolytic enzymes relative to Hb. Daphnia pulicaria from four lakes appeared to demonstrate one of two strategies in relation to coordination of glycolytic genes and Hb. In some lakes D. pulicaria showed a pronounced induction of Hb without changes in glycolytic enzymes, whereas other lakes showed a blunted Hb response but pronounced glycolytic response. Serial sampling showed the Hb response early in the season (May-June) and a glycolytic response later in the season (September- October). Further studies should include transcriptome analyses exploring if lake-by-lake differences are due to microevolutionary variation or phenotypic responses to different degrees and durations of oxygen stress.
URI for this recordhttp://hdl.handle.net/1974/27798
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