Foul play

“FOR God’s sake and our country’s,” wrote an 18th-century captain in Britain’s navy to the Admiralty in Whitehall, “send copper bottomed ships to relieve the foul and crippled ones.” Copper sheathing, first deployed widely in the 1780s, kept fouling at bay by inhibiting the growth of barnacles, mussels, tube worms and shipworms (actually a type of clam). But even today, when copper has been replaced by modern antifouling paints and wooden hulls have given way to metal ones, ship-fouling is still a problem.

Dealing with it costs billions of dollars a year and often involves toxic chemicals whose use is being progressively restricted. How the larvae of befouling creatures choose where to settle is thus of great interest. A paper just published in the Proceedings of the National Academy of Sciences by Nick Shikuma of San Diego State University and his colleagues sheds some light.

Dr Shikuma studies tubeworms. These shell-forming annelids have become model organisms for students of ship-fouling. Their research has already shown that tubeworm larvae like to attach themselves to surfaces covered with lots of bacteria. But how larvae and bacteria interact is only now being elucidated.

For tubeworms, the cue comes from Pseudoalteromonas luteoviolacea, a bacterium abundant on marine surfaces. Individual Pseudoalteromonas cells produce small spears, called phage-tails, to defend themselves against hostile bacteria. But phage-tails also induce metamorphosis in several types of larvae, including tubeworms’. Shortly after contact with a phage-tail, a larva slows down and settles. Within 30 minutes it loses its cilia, the tiny hairs it employs to swim. Soon thereafter, it begins to elongate and to secrete its characteristic calcium carbonate tube around itself.

Dr Shikuma suspected, however, that more than mere mechanical contact with phage-tails was involved in this process. To test his theory, he exposed tubeworm larvae to a suspension of Pseudoalteromonas. As expected, they began to settle down. Then, before they had lost their cilia, he removed the bacteria. Instead of continuing to metamorphose, the larvae backpeddled on the process and began swimming again in search of a new home. Clearly, the initial contact had not triggered an irreversible change; the continued presence of the bacteria was necessary for metamorphosis to go all the way.

Dr Shikuma then tinkered with Pseudoalteromonas’s genes to try to work out what was going on. First, he deleted the part of the bug’s DNA involved in phage-tail production. As he expected, larvae exposed to these mutant bacteria did not even begin to metamorphose. Further tinkering, though, revealed a second set of genetic triggers. Bacteria that had intact phage-tail genes, but had had a block of six other genes deleted, were able to induce larvae to settle down, but not to shed their cilia and complete their metamorphosis. What these genes do for Pseudoalteromonas is not known. But whatever it is they are producing, it clearly also acts as a “go” signal to larvae that all is well for them to complete their metamorphosis.

The discovery of this second pathway opens up an additional biochemical line of attack in the war against fouling. Once the signal the six newly identified genes are producing has been decoded, ways to interfere with it might be devised. That may lead to an environmentally friendly method of stopping sessile marine organisms growing in the wrong places. Even if it does not, Dr Shikuma’s approach seems likely reveal other weak points in the metamorphic process that can be exploited—both saving shipowners money and also saving the oceans from toxic chemicals.