Open AccessRegulation of Anti-Plasmodium Immunity by a LITAF-like Transcription Factor in the Malaria Vector Anopheles gambiae
Author(s) -
Ryan C. Smith,
Abraham G. Eappen,
Andrea J. Radtke,
Marcelo JacobsLorena
Publication year - 2012
Publication title -
plos pathogens
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.719
H-Index - 206
eISSN - 1553-7374
pISSN - 1553-7366
DOI - 10.1371/journal.ppat.1002965
Subject(s) - anopheles gambiae , biology , plasmodium (life cycle) , malaria , innate immune system , transcription factor , anopheles , immune system , vector (molecular biology) , immunity , rna interference , virology , microbiology and biotechnology , gene , parasite hosting , genetics , immunology , rna , world wide web , computer science , recombinant dna
The mosquito is the obligate vector for malaria transmission. To complete its development within the mosquito, the malaria parasite Plasmodium must overcome the protective action of the mosquito innate immune system. Here we report on the involvement of the Anopheles gambiae orthologue of a conserved component of the vertebrate immune system, LPS-induced TNFα transcription factor ( LITAF ), and its role in mosquito anti- Plasmodium immunity. An. gambiae LITAF -like 3 ( LL3 ) expression is up-regulated in response to midgut invasion by both rodent and human malaria parasites. Silencing of LL3 expression greatly increases parasite survival, indicating that LL3 is part of an anti- Plasmodium defense mechanism. Electrophoretic mobility shift assays identified specific LL3 DNA-binding motifs within the promoter of SRPN6 , a gene that also mediates mosquito defense against Plasmodium . Further experiments indicated that these motifs play a direct role in LL3 regulation of SRPN6 expression. We conclude that LL3 is a transcription factor capable of modulating SRPN6 expression as part of the mosquito anti- Plasmodium immune response.