Abstract
The mosquito immune system is involved in pathogen-elicited defense responses. The NF-κB factors REL1 and REL2 are downstream transcription activators of Toll and IMD immune pathways, respectively. We have used genome-wide microarray analyses to characterize fat-body-specific gene transcript repertoires activated by either REL1 or REL2 in two transgenic strains of the mosquito Aedes aegypti. Vitellogenin gene promoter was used in each transgenic strain to ectopically express either REL1 (REL1+) or REL2 (REL2+) in a sex, tissue, and stage specific manner. There was a significant change in the transcript abundance of 297 (79 up- and 218 down-regulated) and 299 (123 up- and 176 down-regulated) genes in fat bodies of REL1+ and REL2+, respectively. Over half of the induced genes had predicted functions in immunity, and a large group of these was co-regulated by REL1 and REL2. By generating a hybrid transgenic strain, which ectopically expresses both REL1 and REL2, we have shown a synergistic action of these NF-κB factors in activating immune genes. The REL1+ immune transcriptome showed a significant overlap with that of cactus (RNAi)-depleted mosquitoes (50%). In contrast, the REL2+ -regulated transcriptome differed from the relatively small group of gene transcripts regulated by RNAi depletion of a putative inhibitor of the IMD pathway, caspar (35 up- and 140 down-regulated), suggesting that caspar contributes to regulation of a subset of IMD-pathway controlled genes. Infections of the wild type Ae. aegypti with Plasmodium gallinaceum elicited the transcription of a distinct subset of immune genes (76 up- and 25 down-regulated) relative to that observed in REL1+ and REL2+ mosquitoes. Considerable overlap was observed between the fat body transcriptome of Plasmodium-infected mosquitoes and that of mosquitoes with transiently depleted PIAS, an inhibitor of the JAK-STAT pathway. PIAS gene silencing reduced Plasmodium proliferation in Ae. aegypti, indicating the involvement of the JAK-STAT pathway in anti-Plasmodium defense in this infection model.
Highlights
Mosquito-borne diseases cause tremendous morbidity and mortality worldwide [1]
The yellow fever mosquito Aedes aegypti is the principal vector of Dengue fever and, due to a large body of knowledge amassed for this mosquito and readily available genetic and molecular tools, it serves as an outstanding model for vector biology [2]
A combination of the genome-wide microarray and transgenic approaches has permitted us to decipher repertoires of genes controlled by two major immune pathways, Toll and IMD, in the Dengue-fever mosquito vector Aedes aegypti
Summary
New approaches to control vector-borne diseases include interruption of the association between pathogens and vectors by genetic manipulation of vectors and the development of transmission-blocking vaccines. Potential success of these approaches requires in-depth knowledge of the molecular interactions between vectors’ defense mechanisms and the evolutionary established ability of a pathogen to overcome these defenses. Despite being five times larger than the genome of the malaria mosquito Anopheles gambiae, the Ae. aegypti genome consists of a similar number of protein-encoding genes, around 17,700 [3,4]. Similar to Drosophila, mosquito Toll and IMD pathways constitute major immune pathways activating a battery of anti-microbial peptides and immune proteins in response to invasion by various
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