摘要：SummaryPhysiological 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 aGCTL-3−/−mutantAedes aegyptiusing CRISPR/Cas9 to investigate the role ofGCTL-3in 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 ofAttacinandGambicin, two targets of the AMPs pathway, partially rescued this reduction in reproductive capabilities. Upregulation of immune response followingGCTL-3knock-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.Graphical AbstractDisplay OmittedHighlights•mosGCTL-3mutants showed a reduced DENV-2 infection rate•mosGCTL-3mutants had upregulated JAK/STAT, IMD, Toll, and AMPs pathway components•mosGCTL-3knock-out led to reduced gut microbiota population sizes, and diversity•mosGCTL-3regulates germ line development and influences fertilityBiological Sciences; Immunology; Microbiology Parasite
