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In the 1930s the geneticist J.B.S. Haldane offered an explanation of why the gene for sickle-shaped red blood cells, which can produce lethal anemia, persisted in tropical populations. He suggested that the mutation offered a trade-off: although the sickle cells raised the risk of death, they also made a person one tenth as likely to contract malaria—a boon in the mosquito-ridden tropics. His striking idea that an infectious disease can drive evolution can now be directly tested in the laboratory with complex creatures, as reported this summer by Spanish researchers in the Proceedings of the National Academy of Sciences USA.
The team, led by José Luis Martínez, a microbiologist at the Spanish National Center of Biotechnology, and Alfonso Navas, director of the National Museum of Natural Sciences in Madrid, used tiny worms known as Caenorhabditis elegans, a species commonly used as a laboratory model. In 2001 the researchers wanted to check how the worms are normally killed in minutes by the infectious bacterium Pseudomonas aeruginosa. After only a week they found that one petri dish out of 152 was crowded with survivors. “At the beginning, we thought it was a mistake,” Navas says. Subsequent experiments showed that the mutants were not only immune to the bacteria but also subsisted on them. “It is like saying: ‘I am not only able to resist the infection, I also eat the killer,’” Navas explains.
