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The Aedes aegypti doublesex (dsx) gene is a master regulator of sexual differentiation, functioning as the terminal switch in the mosquito's sex determination cascade. It produces sex-specific protein isoforms through alternative splicing: the female-specific isoforms (dsxF) and the male-specific isoform (dsxM). These isoforms are transcription factors containing a conserved DM DNA-binding domain that regulate the expression of downstream genes responsible for sexually dimorphic traits. Since only female mosquitoes are responsible for the transmission of pathogens such as Dengue, Zika, and Yellow Fever viruses, dsx is a high-priority target for population control technologies. Genetic interventions, such as CRISPR/Cas9-based gene drives and RNA interference (RNAi), target the female-specific exons of dsx to induce sterility or lethality in females while leaving males unaffected. This strategy aims to suppress or eliminate local mosquito populations to reduce the burden of vector-borne diseases. However, the deployment of such technologies carries significant safety and ethical considerations, including potential ecological disruptions and the development of genetic resistance.
Targeted gene disruption or silencing to induce female sterility or lethality, leading to population suppression.
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