Impact of trehalose transporter knockdown onAnopheles gambiaestress adaptation and susceptibility toPlasmodium falciparuminfection
Author(s) -
Kun Liu,
Yuemei Dong,
Yuzheng Huang,
Jason L. Rasgon,
Peter Agre
Publication year - 2013
Publication title -
proceedings of the national academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.1316709110
Subject(s) - trehalose , hemolymph , anopheles gambiae , desiccation , malaria , biology , gene knockdown , plasmodium falciparum , transporter , parasite hosting , anopheles , adaptation (eye) , microbiology and biotechnology , biochemistry , ecology , immunology , gene , computer science , world wide web , neuroscience
Anopheles gambiae is a major vector mosquito for Plasmodium falciparum, the deadly pathogen causing most human malaria in sub-Saharan Africa. Synthesized in the fat body, trehalose is the predominant sugar in mosquito hemolymph. It not only provides energy but also protects the mosquito against desiccation and heat stresses. Trehalose enters the mosquito hemolymph by the trehalose transporter AgTreT1. In adult female A. gambiae, AgTreT1 is predominantly expressed in the fat body. We found that AgTreT1 expression is induced by environmental stresses such as low humidity or elevated temperature. AgTreT1 RNA silencing reduces the hemolymph trehalose concentration by 40%, and the mosquitoes succumb sooner after exposure to desiccation or heat. After an infectious blood meal, AgTreT1 RNA silencing reduces the number of P. falciparum oocysts in the mosquito midgut by over 70% compared with mock-injected mosquitoes. These data reveal important roles for AgTreT1 in stress adaptation and malaria pathogen development in a major vector mosquito. Thus, AgTreT1 may be a potential target for malaria vector control.
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