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Cell. 2004 Mar 5;116(5):661-70.

Complement-like protein TEP1 is a determinant of vectorial capacity in the malaria vector Anopheles gambiae.

Author information

1
European Molecular Biology Laboratory, Meyerhofstrasse 1, 69117 Heidelberg, Germany.

Abstract

Anopheles mosquitoes are major vectors of human malaria in Africa. Large variation exists in the ability of mosquitoes to serve as vectors and to transmit malaria parasites, but the molecular mechanisms that determine vectorial capacity remain poorly understood. We report that the hemocyte-specific complement-like protein TEP1 from the mosquito Anopheles gambiae binds to and mediates killing of midgut stages of the rodent malaria parasite Plasmodium berghei. The dsRNA knockdown of TEP1 in adults completely abolishes melanotic refractoriness in a genetically selected refractory strain. Moreover, in susceptible mosquitoes this knockdown increases the number of developing parasites. Our results suggest that the TEP1-dependent parasite killing is followed by a TEP1-independent clearance of dead parasites by lysis and/or melanization. Further elucidation of the molecular mechanisms of TEP1-mediated parasite killing will be of great importance for our understanding of the principles of vectorial capacity in insects.

PMID:
15006349
DOI:
10.1016/s0092-8674(04)00173-4
[Indexed for MEDLINE]
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