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Production and degradation of reactive oxygen species (ROS) are extensively regulated to ensure proper cellular responses to various environmental stimuli and stresses. Moreover, physiologically generated ROS function as secondary messengers that can influence tissue homeostasis. The cap'n'collar transcription factor known as nuclear factor erythroid-derived factor 2 (Nrf2) coordinates an evolutionarily conserved transcriptional activation pathway that mediates antioxidant and detoxification responses in many animal species, including insects and mammals. Here, we show that Nrf2-mediated signaling affects embryo survival, midgut homeostasis, and redox biology in Aedes aegypti, a mosquito species vector of dengue, Zika, and other disease-causing viruses. We observed that AeNrf2 silencing increases ROS levels and stimulates intestinal stem cell proliferation. Because ROS production is a major aspect of innate immunity in mosquito gut, we found that a decrease in Nrf2 signaling results in reduced microbiota growth and Zika virus infection. Moreover, we provide evidence that AeNrf2 signaling also controls transcriptional adaptation of A. aegypti to insecticide challenge. Therefore, we conclude that Nrf2-mediated response regulates assorted gene clusters in A. aegypti that determine cellular and midgut redox balance, affecting overall xenobiotic resistance and vectorial adaptation of the mosquito.

Original publication




Journal article


J Biol Chem

Publication Date





9053 - 9063


Aedes aegypti, NFE2L2, Nrf2, Zika, Zika virus, antioxidant, cap';n';collar, erythroid-derived 2-like factor, flavivirus, insect, insecticide resistance, nuclear factor 2, oxidative stress, stem cell, vectorial competence, Aedes, Animals, Female, Gene Expression Regulation, Genes, Insect, Insect Proteins, Insect Vectors, Insecticide Resistance, Male, NF-E2-Related Factor 2, Oxidation-Reduction, Oxidative Stress, Reactive Oxygen Species, Signal Transduction, Zika Virus, Zika Virus Infection