期刊
SCIENCE
卷 352, 期 6283, 页码 349-353出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aad9279
关键词
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资金
- National Health and Medical Research Council (Australia)
- Australian Research Council
- Indonesian Ministry of Research, Technology, and Higher Education
- U.S. National Institutes of Health [AI031478, RR00052]
- Japanese Society for Promotion of Science (JSPS) KAKENHI [23117004, 26253025]
- Japanese Science and Technology Agency/Japan International Cooperation Agency Science and Technology Research Partnership for Sustainable Development (SATREPS) [10000284]
- Program for Promotion of Basic and Applied Researches for Innovations in Bio-oriented Industry (BRAIN)
- Science and Technology Research Promotion Program for Agriculture, Forestry, Fisheries and Food Industry
- Grants-in-Aid for Scientific Research [26253025] Funding Source: KAKEN
Drug resistance compromises control of malaria. Here, we show that resistance to a commonly used antimalarial medication, atovaquone, is apparently unable to spread. Atovaquone pressure selects parasites with mutations in cytochrome b, a respiratory protein with low but essential activity in the mammalian blood phase of the parasite life cycle. Resistance mutations rescue parasites from the drug but later prove lethal in the mosquito phase, where parasites require full respiration. Unable to respire efficiently, resistant parasites fail to complete mosquito development, arresting their life cycle. Because cytochrome b is encoded by the maternally inherited parasite mitochondrion, even outcrossing with wild-type strains cannot facilitate spread of resistance. Lack of transmission suggests that resistance will be unable to spread in the field, greatly enhancing the utility of atovaquone in malaria control.
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