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Transgenic anopheline mosquitoes impaired in transmission of a malaria parasite

Nature volume 417, pages 452455 (23 May 2002) | Download Citation



Malaria is estimated to cause 0.7 to 2.7 million deaths per year, but the actual figures could be substantially higher owing to under-reporting and difficulties in diagnosis1. If no new control measures are developed, the malaria death toll is projected to double in the next 20 years1. Efforts to control the disease are hampered by drug resistance in the Plasmodium parasites, insecticide resistance in mosquitoes, and the lack of an effective vaccine. Because mosquitoes are obligatory vectors for malaria transmission, the spread of malaria could be curtailed by rendering them incapable of transmitting parasites. Many of the tools required for the genetic manipulation of mosquito competence for malaria transmission have been developed. Foreign genes can now be introduced into the germ line of both culicine2,3 and anopheline4 mosquitoes, and these transgenes can be expressed in a tissue-specific manner5,6. Here we report on the use of such tools to generate transgenic mosquitoes that express antiparasitic genes in their midgut epithelium, thus rendering them inefficient vectors for the disease. These findings have significant implications for the development of new strategies for malaria control.

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  1. 1.

    The ears of the hippopotamus: manifestations, determinants, and estimates of the malaria burden. Am. J. Trop. Med. Hyg. 64s, 1–11 (2001)

  2. 2.

    et al. Stable transformation of the yellow fever mosquito, Aedes aegypti, with the Hermes element from the housefly. Proc. Natl Acad. Sci. USA 95, 3743–3747 (1998)

  3. 3.

    , , & Mariner transposition and transformation of the yellow fever mosquito, Aedes aegypti. Proc. Natl Acad. Sci. USA 95, 3748–3751 (1998)

  4. 4.

    et al. Stable germline transformation of the malaria mosquito Anopheles stephensi. Nature 405, 959–962 (2000)

  5. 5.

    et al. Engineering blood meal-activated systemic immunity in the yellow fever mosquito, Aedes aegypti. Proc. Natl Acad. Sci. USA 97, 9144–9149 (2000)

  6. 6.

    et al. Robust gut-specific gene expression in transgenic Aedes aegypti mosquitoes. Proc. Natl Acad. Sci. USA 97, 10895–10898 (2000)

  7. 7.

    , & The journey of malaria in the mosquito: hopes for the new century. Parasitol. Today 16, 196–201 (2000)

  8. 8.

    , & Targeting Plasmodium ligands on mosquito salivary glands and midgut with a phage display peptide library. Proc. Natl Acad. Sci. USA 98, 13278–13281 (2001)

  9. 9.

    , , & Rapid induction by a blood meal of a carboxypeptidase gene in the gut of the mosquito Anopheles gambiae. Insect Biochem. Mol. Biol. 27, 1063–1072 (1997)

  10. 10.

    A quantitative study of naturally-acquired malaria infections in Anopheles gambiae and Anopheles funestus in a highly malarious area of East Africa. Trans. R. Soc. Trop. Med. Hyg. 60, 626–632 (1966)

  11. 11.

    & A versatile vector set for animal transgenesis. Dev. Genes Evol. 210, 630–637 (2000)

  12. 12.

    & Germline transformation of Drosophila melanogaster with the piggyBac transposon vector. Insect Mol. Biol. 8, 449–457 (1999)

  13. 13.

    , & Highly sensitive, fluorescent transformation marker for Drosophila transgenesis. Dev. Genes Evol. 210, 623–629 (2000)

  14. 14.

    , & Trypsin and aminopeptidase gene expression is affected by age and food composition in Anopheles gambiae. Insect Biochem. Mol. Biol. 26, 651–658 (1996)

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We thank J. Snyder and G. Hundemer for help, and members of the laboratory for comments. This investigation received financial support from the UNDP/World Bank/WHO Special Programme for Research and Training in Tropical Diseases (TDR) and from the National Institutes of Health. E.A.W. acknowledges support by the Robert Bosch Foundation.

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Author notes

    • Junitsu Ito
    •  & Anil Ghosh

    These authors contributed equally to this work


  1. *Case Western Reserve University, Department of Genetics, 10900 Euclid Avenue, Ohio 44106-4955, USA

    • Junitsu Ito
    • , Anil Ghosh
    • , Luciano A. Moreira
    •  & Marcelo Jacobs-Lorena
  2. ‡Lehrstuhl für Genetik, Universität Bayreuth, Universitätsstrasse 30, NW1, D-95447 Bayreuth, Germany

    • Ernst A. Wimmer


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Competing interests

The authors declare that they have no competing financial interests.

Corresponding author

Correspondence to Marcelo Jacobs-Lorena.

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