Moths and butterflies have long fallen victim to two deadly threats: parasitic wasps and viruses, which battle each other over their lepidopteran hosts. Now, a new study shows some viruses transfer their weapons to infected moths and butterflies, arming them with the genes to make parasite-killing proteins.
Many species of wasps and flies lay their eggs inside other insects, giving their young a source of food and a safe place to develop—and killing the host in the process. But even though moths and butterflies are favored hosts, some species, including armyworms, cutworms, and cabbage butterflies, have shown a strange resistance to a plethora of wasp parasites, such as Cotesia vanessae and C. kariyai.
To find out what was going on, entomologist Madoka Nakai and her team at the Tokyo University of Agriculture and Technology infected northern armyworm larvae with a common pox virus before introducing the immature insects to various parasitic wasp species. Whereas uninfected larvae succumbed to the parasites, the infected larvae—and their plasma—killed almost every parasite, aside from the basket-cocoon parasitoid Meteorus pulchricornis. Researchers then identified two proteins in the infected armyworms, which they called parasitoid killing factor (PKF), that they thought might be toxic to the parasites.
Next, insect pathologist Salvador Herrero and colleagues at the University of Valencia found genes in both insect-infecting viruses and moth and butterfly hosts that could make PKFs. An analysis of the lepidopteran family tree suggested the PKF genes were transferred multiple times from the viruses to the lepidopterans. “What doesn’t kill you makes you stronger,” Herrero says. “The insect survived the infection from the virus, acquired one of these genes, and now has protection against another enemy, the parasitoid.”
To show that it was the PKF proteins that were doing the killing, University of British Columbia, Okanagan, molecular biologist David Theilmann and colleagues infected bertha armyworms with two baculovirus species, MacoNPV-A and MacoNPV-B. They found that the infected armyworms successfully resisted braconid wasp larva parasites (C. vanessae). Meanwhile, beet armyworms, whose own genes make PKFs, were also able to kill the parasites. When scientists knocked out the genes that produced the PKFs in the beet armyworms, many more parasites survived, suggesting the PKFs were responsible for the parasite deaths, the researchers write today in Science.
To find out how the PKFs were killing the parasites, scientists exposed braconid wasp larva to beet armyworm and infected northern armyworm plasma. DNA fragments and signaling molecules in exposed cells suggested PKFs had caused affected cells to explode.
“We all arrived at these genes from slightly different directions. Putting our research together created this very interesting story about the biological arms race occurring on a very large scale between multiple pathogens, wasps, and hosts, which we now know are also fighting back,” Theilmann says.
But the researchers also found an interesting twist—at least one of the PKF-harboring viruses is transmitted to moths and butterflies by the basket-cocoon parasitoid, protecting the very wasp whose larvae can survive its assaults. That suggests that even though PKFs can help the lepidopterans, they may also give an advantage to some parasitic wasps.
The new work should help researchers understand why moths and butterflies often resist parasitoids used as pesticides for crops and forests, Herrero says. But when it comes to fully understanding the complexity of this evolutionary arms race, many questions are unanswered, Theilmann says. For example, his team still doesn’t know why some viruses have genes for PKF and others don’t. They also don’t know whether all PKFs function in the same manner.
“I think this is a good first step,” says Michael Strand, an entomologist at the University of Georgia who specializes in parasite-host interactions. By identifying these new proteins, he adds, the new study has paved the way for important future work. Meanwhile, the researchers plan to investigate where these virus-host-parasite interactions typically take place in the wild. They also want to track down PKF’s specific targets—and see whether any other genes play a similar, toxic role.
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