Abstract
Physiological trade-offs between mosquito immune response and reproductive capability can arise due to insufficient resource availability. C-type lectin family members may be involved in these processes. We established a GCTL-3(-/-) mutant Aedes aegypti using CRISPR/Cas9 to investigate the role of GCTL-3 in balancing the costs associated with immune responses to arboviral infection and reproduction. GCTL-3(-/-) mutants showed significantly reduced DENV-2 infection rate and gut commensal microbiota populations, as well as upregulated JAK/STAT, IMD, Toll, and AMPs immunological pathways. Mutants also had significantly shorter lifespans than controls and laid fewer eggs due to defective germ line development. dsRNA knock-down of Attacin and Gambicin, two targets of the AMPs pathway, partially rescued this reduction in reproductive capabilities. Upregulation of immune response following GCTL-3 knock-out therefore comes at a cost to reproductive fitness. Knock-out of other lectins may further improve our knowledge of the molecular and genetic mechanisms underlying reproduction-immunity trade-offs in mosquitoes.