ROS RELOCATES MOUTHS

Abstract

The trick to making the most of your mouth is keeping it close to food,which isn't a problem if you can pick yourself up and wander over to the next meal. But life isn't that straightforward for simple hydroids that make their homes on rocks and other creature's shells. Where ever food appears, they have to grow feeding structures at the food source `otherwise they'll have a short and unhappy life', says Neil Blackstone. But how does the presence of food trigger this response at a time of plenty? Knowing that some organisms signal metabolic changes with reactive oxygen species generated by their mitochondria, Blackstone wondered if the hydroid colonies might be using the same signalling approach to control where they place their mouths. By altering reactive oxygen species generation at key mitochondrial sites and watching how the colonies grew in response, Blackstone has evidence that reactive oxygen species play a signalling role in hydroid colony development(p. 651).A hydroid colony only needs a few happily feeding polyps to supply nutrition to the rest of the colony. Muscular structures at the base of the feeding polyp contract, consuming energy to pump the food to the rest of the colony's inhabitants. As the feeding polyp's metabolic demand rises, a chain of electron transporting proteins maintains the ATP-generating proton gradient across the mitochondria's membrane. But some of the electrons are picked up from the electron transport chain by oxygen molecules to generate reactive oxygen species such as peroxide. As the feeding polyp's metabolic demand rises it produces less reactive oxygen species, while polyps that are further from the food source have a lower metabolic demand and consequently higher levels of reactive oxygen species. Which made Blackstone suspect that the reactive oxygen species' gradient could regulate the polyps' development.Blackstone decided to manipulate the levels of ROS produced by the hydroid's mitochondria with drugs to see if altered ROS levels affected the way a hydroid colony developed. Taking genetically identical hydroid colonies,Blackstone watched how they grew as he altered their ROS levels. Sure enough,colonies that produced high and low levels of ROS developed as he had expected, with colonies that produced low levels of ROS developing densely packed structures with many mouths. So mitochondrially generated ROS probably carried part of the signal that drove the colonies' development. But Blackstone was puzzled when he looked at colonies that were treated with a drug that should have produced intermediate levels of ROS; they developed as if low ROS levels were signalling another feast on hand. However, Blackstone explains that this apparently confusing result might help him to close in on the point in the electron transport chain where the developmental signal originates.