Aedes aegypti vision-guided target recognition requires two redundant rhodopsins

Abstract

AbstractBlood-feeding insects, such as the mosquito, Aedes (Ae.) aegypti, use multiple senses to seek out and bite humans [1, 2]. Upon exposure to CO2, the attention of female mosquitoes to potential human targets is greatly increased. Female mosquitoes use vision to assist them in honing in on hosts that may be up to 10 meters away [3–9]. Only after coming into close range do convective heat from skin and odors from volatile organic compounds come into play, allowing female mosquitoes to evaluate whether the object of interest might be a host [10, 11]. Here, using CRISPR/Cas9 we mutated the gene encoding Op1, which is the most abundant of the five rhodopsins expressed in the compound eyes of Ae. aegypti. Using a cage assay and a wind tunnel assay, we surprisingly found that elimination of op1 did not impair CO2-induced target seeking. We then mutated op2, which encodes the rhodopsin most similar to Op1, and also found that there was no impact on this behavior. Rather, mutation of both op1 and op2 was required to abolish vision-guided target recognition. In contrast to this defect, the double mutants still exhibited normal light attraction. By measuring the optomotor response, we found that the double mutants still recognized moving cues in their environment. In further support of the conclusion that the double mutant is not blind, we found that the animals retained an electrophysiological response to light, although it was diminished. This represents the first perturbation of vision in mosquitoes and indicates that hostseeking by Ae. aegypti depends on redundant rhodopsins.