Deoller 9728409 Hydrogen sulfide, a common constituent of several natural and man-made aquatic habitats, is both a potent toxin of aerobic cellular respiration and an electron-rich molecule used by some bacteria as an energy source. In ciliated gills from Geukensia demissa, a marine mussel from sulfide rich sediments, sulfide oxidation supports cellular work, indicating for the first time that in an intact metazoan tissue, mitochondria switch from carbon catabolism to sulfide oxidation for energy production. In this project, using excised intact G. demissa gills and isolated gill mitochondria, three central questions concerning the transition from carbon catabolism to sulfide oxidation will be addressed: what is the nature of this transition; what factors regulate it; and, since sulfide exposure history influences capacity for sulfide oxidation, what mechanism(s) underlies this alternation in capacity? The results of this work will help rigorously address a long-standing question, namely how do organisms adapt to sulfide exposure? The findings may indicate that energy budgets of ecosystems containing sulfide habitats need reconsideration if sulfide oxidation can result in carbon sparing in metazoans. Assessment of mitochondrial function using innovative and state-of-the-art techniques will further our understanding of this possibly widespread adaptation to seemingly in hospitable environments.
