BLACKSTONE, N.W.: Redox State, Reactive Oxygen Species (ROS), and Adaptive Growth of Hydroid Colonies

Redox chemistry, involving the transfer of electrons and hydrogen atoms, is central to energy conversion in respiration, and control of gene expression by redox state commonly occurs in bacteria, allowing rapid response to environmental changes. Colonial hydroids often encrust surfaces over which the food supply varies in time and space; hence, in these organisms redox control of the development of feeding structures (polyps) and gastrovascular connections (stolons) could be similarly adaptive, allowing colonies to adjust the timing and spacing of these structures in response to a variable food supply. Feeding triggers strong contractions of polyp epitheliomuscular cells, resulting in high rates of gastrovascular flow. In fed polyps, this metabolic demand shifts the redox state of these cells in the direction of oxidation and diminishes the rate of formation of mitochondrial ROS. On the other hand, after 24 h without food, polyp epitheliomuscular cells become quiescent, redox state shifts in the direction of reduction, and formation of mitochondrial ROS increases. Perturbations of redox state and ROS can also be initiated using uncouplers of oxidative phosphorylation and inhibitors of the mitochondrial electron transport chain. The effects on colony pattern formation are similar: relative oxidation results in high rates of polyp and stolon tip initiation, while relative reduction results in low rates. As in other systems, ROS may mediate the effects of redox state: high levels of ROS may suppress the gene activity that leads to polyp and stolon tip initiation, while low levels of ROS may be permissive in this regard. In this way, metabolic demand, redox state, and ROS may interact to control pattern formation in hydroid colonies and to allow adaptive growth forms in response to the food supply and other environmental factors.