Transmission begins in the gut.

Sexual dimorphism in disease vectors is usually studied in the reproductive tract. But the midgut is dimorphic too — only females take blood, and only female guts do the physiology that follows. We work on how sex-determination genes, doublesex among them, specify that tissue. Knocking down female doublesex by oral RNAi reduces both the number and the fitness of adult female Anopheles gambiae, which makes this pathway a control target as well as a developmental question. We are working in both Aedes and Anopheles to determine the sex-specific determinants of cell identity in the gut.

Our proposal for a spatial single-cell atlas of the female midgut earned an honorable mention in the 10x Genomics Core Lab Grant, and the pilot is now going ahead with them — Visium HD and single-nucleus sequencing, resolving the tissue region by region and cell type by cell type.

Mating changes far more than the reproductive tract. In Aedes aegypti, mating and juvenile hormone drive midgut growth and dampen the antimicrobial peptide response — and with immunity turned down, a native bacterial population takes hold. Mosquitoes carrying it lay more eggs and live longer. We are mapping the steps between the hormonal cue and the remodeled tissue, and asking what that immune trade-off costs in vector competence.

No two blood meals are the same. Composition shifts with the host, and the midgut has to digest, detoxify and rebuild against whatever arrives. The epithelium answers by adjusting proliferation and endoreplication — some cells divide, others copy their genome without dividing and grow instead. We are working out which components of the meal trigger that switch, and how the balance between the two routes sets the tissue's capacity to handle damage and infection.