Spite’s roots
Spite seems to be a uniquely human phenomenon, but examining interactions among organisms you’d never peg as vengeful is giving scientists some insight into how the rather nasty behavior arose. It’s difficult to see how spite could evolve: what benefit is there in punishing another party at the cost of harming one’s own reproductive fitness? “Six years ago, no one thought it was possible,” says Oxford University evolutionary biologist Stuart West. Some researchers have suggested that natural selection can favor spite if the recipient is less related to the actor than would be expected by chance. But this circumstance would not be widespread in nature, limited to small populations or to social insect colonies where sterile workers and soldiers have nothing to lose in terms of individual reproductive fitness.
Hadas Hawlena, a postdoc in evolutionary biologist Curt Lively’s Indiana University lab, became interested in a different hypothesis for the evolution of spiteful behavior. The hypothesis proposes that the spatial distribution of a species might allow spite to evolve, where genetically diverse individuals from different populations—different strains of the same species—come into contact with each other along the boundaries of their territory. Hawlena was intrigued when her colleagues discovered that some laboratory bacteria released bacteriocins, toxins that can kill closely related strains of the same species and are equally toxic to the emitters. She searched the literature but could not find any evidence that bacteriocin-mediated interactions are important in nature.
“I decided to go into the field and find out myself,” Hawlena says. She and her colleague Farrah Bashey went to the Indiana University Research and Teaching Preserve at Moore’s Creek, where Bashey had previously isolated bacteriocin-producing bacteria. At first, they had no idea where to look, so the two simply took samples based on a uniform grid laid out on the soil, unsure whether their target bacteria were present.
They were interested in a couple of bacterial species belonging to genus Xenorhabdus, which are symbiotic with the insect-dwelling nematode Steinernema carpocapsae. After infecting an insect, the nematodes release the bacteria, which grow rapidly, killing the insect within a few days. Then the nematodes reproduce within the insect’s body, and 2 weeks later thousands of young worms, each carrying an inoculum of bacteria, strike out in search of new insect hosts. An individual worm may travel a few meters to find an insect to infect.
Back in the lab, Hawlena and Bashey divided the soil samples into separate Petri dishes, placing three caterpillars into each dish. If any of the caterpillars died, they transferred the corpse to a trap that would collect the young nematodes and extract bacteria from them—10 Xenorhabdus colonies from each worm. They watched each dish every day for 6 months and spent another 8 months optimizing the bacteriocin assay.
Hawlena tested the isolated bacterial colonies by treating them with a compound called mitomycin C, which induces bacteriocin production, to see if the resulting extracts could shut down their neighbors’ growth. She found that neighbors living up to a meter apart on a hill at the creek preserve were closely related on a genetic level and were living peacefully together. Strains that had been living a few meters apart were not only less genetically related, but would readily (and spitefully) poison each other’s colonies (Evolution, doi: 10.1111/j.1558-5646.2010.01070.x, 2010).
Hawlena’s research complements laboratory bacteriocin work, West says, taking research into spite “to the next level, by moving into the field in a sensible and clear way.” Though she was skeptical of finding bacteriocin-related interactions in the field, and didn’t expect high levels of genetic diversity at these relatively small scales, Hawlena has lent support to the hypothesis: the further away bacteria get from their “hometown,” the less related they are, and the more spiteful they become. “We were surprised and amazed to see that this is exactly what happens in nature,” she says. Faculty Member Rachel Norman of Stirling University, who selected the paper for Faculty of 1000, wrote that she was impressed by “the close relationship between modeling and experiments that was presented.”
But Hawlena doesn’t want to stop there. She believes she can easily replicate the work with human gut bacteria or in disease vectors such as ticks. Hawlena plans to repeat the competition assays on Xenorhabdus within the caterpillar itself, to see if the spiteful interactions indeed determine which species wins out, and how this might affect the mortality of the host.
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