Liquefying virus uses one gene to make caterpillars climb

ByEd Yong
September 08, 2011
5 min read

It is dawn in a European forest, and gypsy moth caterpillars are looking for somewhere to hide. With early birds starting to rise, the caterpillars will spend the day in bark crevices or buried in soil. But one of them is behaving very strangely. While its peers head downwards, this one climbs upwards, to the very top of the highest leaves. It has come to die.

At the top of its plant, the caterpillar liquefies. Its body almost seems to melt. As it does, it releases millions of viruses, dripping them onto plants below and releasing them into the air. These viruses are the agents that compelled the caterpillar to climb, and eventually killed it. They are baculoviruses, and they cause a condition known aptly as Wipfelkrankheit – the German for “tree top disease”.

By ensuring that their hosts die in a high spot, the viruses benefit in two ways. First, that’s where uninfected caterpillars pupate and turn into adults. Female gypsy moths don’t fly. When they emerge, they walk over the same bark and leaves that their infected peers, now dead and molten, have laced with viruses. They risk infection with every footfall, and they might even contaminate their own eggs. The high position also allows the viruses to spread on gusts of wind. They can travel over long distances before descending upon fresh hosts in bursts of infectious rain.

Scientists have known about Wipfelkrankheit for over a century, but they’re only starting to unpick its details. For example, Kelli Hoover and Michael Grove from Pennsylvania State University have just discovered one of the genes that one baculovirus – LdMNPV – uses to control its moth hosts.

The gene is called egt. When Hoover and Grove removed it, the virus still managed to kill its caterpillars, but it couldn’t make them climb. Instead, the insects perished at a lowly position at the bottom of their containers. When Hoover and Grove reinserted the gene into their altered virus, they restored its ability to change the caterpillars’ behaviour.

The egt gene inactivates 20E, a caterpillar hormone that controls moulting. When it’s time for the caterpillar to slough off its outer skin, its levels of 20E go up and it climbs to a high position. Hoover thinks that the virus inactivates just enough of the hormone to make the caterpillars climb without actually triggering a moult. The insect goes to the right spot, but instead of shedding its skin, it dies.

This is a great example of what Richard Dawkins calls “the extended phenotype” – where genes can influence events well beyond the bodies that they live in. Beaver genes, for example, not only influence the bodies of beavers, but the construction of dams and the shape of entire river systems. Most of the examples that Dawkins cites cannot be traced back to specific genes. Hoover and Grove have found an exception – a single virus gene that can control the behaviour of another animal.

The baculoviruses are just some of the many parasites that change the behaviour of their hosts, and many of them trigger unusual tendencies to climb. The fungus Cordyceps unilateralis drives ants to bite into leaves around 25 centimetres above the forest floor. This zone has the perfect conditions for the fungus to develop its spore capsule, which erupts fatally through the ant’s head. Meanwhile, the Leucochloridium fluke cancels out a snail’s fear of bright lights, driving them to open spaces where they’re more readily eaten by birds – the fluke’s final host. Perhaps someday, scientists will decipher the genes that allow these parasites to take over minds as well as bodies.

Reference: Hoover, Grove, Gardner, Hughes, McNeil, Slavicek. 2011. A Gene for an Extended Phenotype. Science http://dx.doi.org/10.1126/science.1209199

Images all courtesy of Michael Grove

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