Of beetles and bacteria

Infected pine, with trails created by female beetles. The white pods are larvae deposited by females.

Erich G. Vallery / USDA Forest Service—SRS-4552, US

All across the United States and Canada, tiny pine bark beetles are killing trees. From the northern pine bark beetle in Canada, the mountain pine bark beetle in Colorado, Montana, and Idaho to the southern pine bark beetle in the southeastern United States, this bug—only millimeters in length—is costing North America tens of millions of dollars each year.

But the beetles' hold on their habitat is not iron-clad—one, the southern pine bark beetle (Dendroctonus frontalis)—depends on the light touch of a mutualistic microbe, Entomocorticium sp. A, to feed its larvae. And as Jon Clardy of Harvard Medical School and Cameron Currie of the University of Wisconsin-Madison discovered, for this species the old adage "the enemy of my enemy is my friend" rings true—perhaps leading to new tools to control these tree-killers and other pathogens that infect humans.

Collaboration began when, as Clardy says, "I became acquainted with [Currie's] work through the literature and began to pester him to work together."

Clardy was intrigued by Currie's findings in his studies of leaf cutter ants (Atta sexdens), and the complicated relationship the ants enjoy with the fungi they nourish and tend as a food source. What particularly interested Clardy was Currie's discovery that organisms use microbes to ward off damage from harmful species (other microbes, in fact), while leaving helpful species alone (Biol Lett, 2:12–16, 2006).

When the pair put their heads together to study D. frontalis, they discovered the same phenomenon. Specifically, the beetle carries a bacterium that produces an antifungal that attacks an antagonistic fungus—Ophiostoma minus—but leaves Entomocorticium sp. A relatively unscathed. They dubbed the new antifungal mycangimycin because of its location in the mycangium of the beetle (Science, 322:63, 2008).

Interestingly, other fungi—including two human pathogens, Candida albicans and Aspergillus nidulans—appear sensitive to mycangimycin. However, Clardy says he does not think mycangimycin will prove useful as an antifungal agent. "For one thing, the molecule has terrible stability and other problems, and I can't imagine anyone's developing it as a drug," he writes in an email. "What mycangimycin could be useful for is identifying targets that could kill fungi—targets that are different from those that we now know." Studying the antifungal's mode of action will reveal its target, which could point to other molecules that hit the same target, "a not uncommon way in which natural products like mycangimycin are used to discover drugs."  

Nancy Moran, professor of ecology and evolutionary biology at the University of Arizona in Tucson, agrees. "These close interactions are the exact place to look for potent bioactive molecules that might be of use in different contexts, such as medicine and pest control," she says in an email. "The very fact that the toxin is deadly to one fungus and harmless to the mutualistic fungus indicates that such molecules can be used in very targeted ways."

When asked if he agrees that these findings could point the way to new biological controls to eradicate the pest, Currie, a native of Canada, simply sighs and says: "I hope so."