Unless you're in the Dead Sea, where the salty water makes floating easy,you'll have to put some effort into staying afloat. Likewise, staying at a constant depth below the sea's surface takes a lot of effort. For fish,putting in effort to maintain their depth in the sea would make finding prey or avoiding predators even more difficult than it already is. To get around this problem many fish have resorted to using a wide variety of strategies to achieve neutral buoyancy. This has clear advantages; since neutrally buoyant fish don't have to work to maintain a particular depth, their muscles are free to perform other behaviours.
Of the many innovations that fish use to achieve neutral buoyancy, the gas-inflated swimbladder is perhaps the most striking. However, the swimbladder doesn't work alone; it requires several other physiological and anatomical innovations, including a network of capillaries called the rete mirabile that's responsible for increasing the amount of dissolved oxygen around the swimbladder, which diffuses into and inflates the swimbladder.
How did these innovations evolve? That's the question Michael Berenbrink and colleagues at the University of Liverpool set out to answer in a recent Science article. They started by focussing on the evolution of another rete that's responsible for getting oxygen to the fish's eye. Mapping the presence and absence of the eye rete onto a fish phylogeny, the team showed that it evolved once, about 250 million years ago. When they mapped the presence and absence of the swimbladder reteonto the same phylogeny, they found it evolved several times, but only after the fish already had the eye rete.
But how do the retia deliver their oxygen loads to the eye and swimbladder against an oxygen gradient? It turns out that fish have a special form of haemoglobin that shows a Root effect; that is, in acidic conditions its oxygen affinity changes and it offloads oxygen, even at high oxygen tensions. Since this special form of haemoglobin would appear to be necessary for the retia to function properly, the team reasoned that it must have evolved before the first rete - the eye rete -appeared. To find out, Berenbrink and his colleagues measured the Root effect in 49 fish species and mapped this onto their phylogeny. Sure enough, they found that this Root-effect haemoglobin evolved only once, before the evolution of the eye rete. They point out that those fish that have lost the eye and swimbladder retia also show reductions in their Root effect, suggesting that the need for oxygen delivery maintains the Root effect in fish.
Having Root-effect haemoglobins in their bloodstream presents an interesting problem for fish; exercise and hypoxia lead to increased blood acidity levels, which may cause haemoglobins with strong Root effects to offload their oxygen in inappropriate places. Berenbrink and his colleagues discovered that another innovation apparently evolved to protect fish from this eventuality: a sodium-proton exchanger that regulates acidity in red blood cells. They show that this exchanger's activity increased after the eye rete evolved and its activity is reduced when the eye reteis secondarily lost. This suggests that the exchanger probably evolved to solve fishes' acidity-regulation problem.
This analysis by Berenbrink and his team provides insights into the evolution of a unique suite of anatomical and physiological innovations that may have contributed significantly to the buoyant success of the ∼22,000 bony fish species alive today.
