About 100 million years ago, the bacterium Wolbachia came up with a trick that has made it one of the most successful parasites in the animal kingdom: It evolved the ability to manipulate the sex lives of its hosts.
“When it developed this capability, Wolbachia spread rapidly among the world’s populations of insects, mites, spiders and nematodes, producing the greatest pandemic in the history of life,” says Seth Bordenstein, assistant professor of biological sciences, who is studying the relationship between this parasitic bacteria and Nasonia, a genus of small wasps that preys on various species of flies.
Bordenstein is a member of the Nasonia Genome Working Group, a collaboration of scientists who published the complete genomes of three species of Nasonia in the Jan. 15 issue of the journal Science. The group identifies several genes that the wasps appear to have picked up from the bacteria.
This new genetic information has allowed Bordenstein to identify one of the key tools in the bacterium’s bag of tricks. It causes a gene in the wasp’s immune system to produce less of the protein responsible for detecting bacterial intruders and issuing the chemical alarm signal that activates the wasp’s various defense mechanisms. This hijacking of the immune system allows the bacterium to invade the bodies of its hosts with relative impunity, he proposes.
Exactly how the bacterium alters its hosts’ reproductive systems to its advantage remains a matter for future study. But scientists have identified the bacterium’s basic strategies. Depending on its host, the bacterium either:
- Kills infected males;
- Feminizes infected males so they develop as females or infertile pseudo-females;
- Induces parthenogenesis (the reproduction of infected females without males); or
- Makes the sperm of infected males incompatible with the eggs of uninfected females or females infected with a different Wolbachia strain.
Wolbachia favors female over male offspring because they are present in mature eggs, but not in mature sperm. As a result, only infected females pass on the infection to their offspring. “This makes them the ultimate feminist weapon,” says Bordenstein.
Although the bacterium’s parasitism is limited to arthropods—animals with exoskeletons instead of backbones—its prevalence has a major impact on the biosphere. According to one study, more than 16 percent of insect species in South and Central America, Mexico, the Caribbean Islands and southern Florida are infected, and as many as 70 percent of all insect species are potential hosts.
Recognition of Wolbachia’s capabilities has made it a promising candidate for genetic engineers who are looking for ways to fight human diseases spread by insects. “Once we understand how Wolbachia works, we should be able to add some genes that allow us to control insects that vector human diseases like malaria and dengue fever,” says Bordenstein. Several research projects supported by the Gates Foundation and the National Institutes of Health are pursuing this idea.
Although the ubiquitous bacteria cannot trick the human immune system, it does have an adverse impact on human health. For example, it infects many species of nematodes, including the filarial nematodes that infect more than 200 million people worldwide, causing debilitating inflammatory diseases such as river blindness and elephantiasis.
During the past 10 years, scientists have realized that it is actually the bacteria, not the nematode, that are responsible for most symptoms produced by these illnesses. Although Wolbachia can only survive about three days in the human body, the parasitic nematodes act as a continuing source of the bacteria that cause most of the damage. This surprising insight has improved the treatment of these illnesses: They are now treated with an antibiotic that kills the bacteria and is less toxic than anti-nematode medications.
Bordenstein’s research was supported by a grant from the National Institutes of Health, and the genome sequencing was funded by the National Human Genome Research Institute.
Find out more: http://bordensteinlab.vanderbilt.edu