First published online September 23, 2003
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.
(2003 ), 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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© The Company of Biologists Ltd 2003