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First published online September 23, 2003
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Towards genetic manipulation of wild mosquito populations to combat malaria: advances and challenges

Michael A. Riehle, Prakash Srinivasan, Cristina K. Moreira and Marcelo Jacobs-Lorena*

Johns Hopkins University, Bloomberg School of Public Health, Dept of Molecular Microbiology & Immunology, 615 N. Wolfe St, Baltimore, MO 21205-2179, USA



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Fig. 1. Life cycle of Plasmodium in the mosquito. The approximate developmental time at which each stage occurs in Plasmodium berghei (maintained at 20°C) is indicated. Transmission starts when the mosquito ingests an infected bloodmeal (0 h). Within minutes, gametocytes develop into gametes (the star-shaped figure illustrates exflagellation, which is the formation of male gametes) that fuse to form the zygote. At 24 h, the motile ookinete invades the midgut epithelium and differentiates into an oocyst. About 2 weeks later, the oocyst ruptures, releasing thousands of sporozoites into the mosquito body cavity. Of all the tissues that sporozoites come in contact with, they can invade only the salivary gland. When the mosquito bites another vertebrate host, transmission is completed by release of sporozoites from the salivary glands (not shown). Reprinted from Ghosh et al. (2003Go), with permission from Elsevier Science.

 


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Fig. 2. Transgenic An. stephensi mosquitoes expressing the dsRED marker. (A) Fluorescence photomicrographs of transgenic fourth instar larva, viewed from the ventral side. Top, dsRED fluorescence alone; bottom, fluorescence superimposed on a light micrograph. dsRED expression is regulated by the 3xP3 promoter, which is active in the eyes and nervous system. (B) Fluorescence photomicrographs of an adult head viewed from the ventral side (left, fluorescence only; right, merged fluorescence and light micrograph). Note that all ommatidia express the dsRED marker, but because fluorescence depends on the angle of the incident (activating) light, only a few are visible in the photo.

 





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