The midgut of insect vectors of human disease contains not only pathogens harmful to human health, but also a diverse microbiota. This microbiota can influence insects’ susceptibility to human pathogens, and the capacity to transmit them, through different mechanisms. Understanding the interaction between the vector, its microbiota and transmitted pathogens will provide novel opportunities to limit disease transmission.
The molecular pathways controlling gender are highly variable and have been identified in only a few nonmammalian model species. In many insects, maleness is conferred by a Y chromosome-linked M factor of unknown nature. We have isolated and characterized a gene, Yob, for the M factor in the malaria mosquito Anopheles gambiae Yob, activated at the beginning of zygotic transcription and expressed throughout a male's life, controls male-specific splicing of the doublesex gene. Silencing embryonic Yob expression is male-lethal, whereas ectopic embryonic delivery of Yob transcripts yields male-only broods. This female-killing property may be an invaluable tool for creation of conditional male-only transgenic Anopheles strains for malaria control programs.
Invasion of the malaria vector Anopheles gambiae midgut by Plasmodium parasites triggers transcriptional changes of immune genes that mediate the antiparasitic defense. This response is largely regulated by the Toll and Immune deficiency (IMD) pathways. To determine whether An. gambiae microRNAs (miRNAs) are involved in regulating the anti-Plasmodium defense, we showed that suppression of miRNA biogenesis results in increased resistance to Plasmodium falciparum infection. In silico analysis of An. gambiae immune effector genes identified multiple transcripts with miRNA binding sites. A comparative miRNA microarray abundance analysis of P. falciparum infected and naïve mosquito midgut tissues showed elevated abundance of miRNAs aga-miR-989 and aga-miR-305 in infected midguts. Antagomir inhibition of aga-miR-305 increased resistance to P. falciparum infection and suppressed the midgut microbiota. Conversely, treatment of mosquitoes with an artificial aga-miR-305 mimic increased susceptibility to P. falciparum infection and resulted in expansion of midgut microbiota, suggesting that aga-miR-305 acts as a P. falciparum and gut microbiota agonist by negatively regulating the mosquito immune response. In silico prediction of aga-miR-305 target genes identified several anti-Plasmodium effectors. Our study shows that An. gambiae aga-miR-305 regulates the anti-Plasmodium response and midgut microbiota, likely through post-transcriptional modification of immune effector genes.
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