Insects fight
infection using a variety of signaling pathways and immune effector
proteins. In Drosophila melanogaster, three members of the
Nimrod gene family (draper, nimC1 and eater) bind bacteria, and this binding leads to phagocytosis by hemocytes. The
Nimrod gene family has since been identified in other insects, but their function in non-drosophilids remains unknown. The purpose of this study was to identify the members of the
Nimrod gene family in the
malaria mosquito, Anopheles gambiae, and to assess their role in immunity. We identified and sequenced three members of this gene family, herein named draper,
nimrod and eater, which are the orthologs of D. melanogaster draper, nimB2 and eater, respectively. The three genes are preferentially expressed in hemocytes and their peak developmental expression is in pupae and young adults.
Infection induces the transcriptional upregulation of all three genes, but the magnitude of this upregulation becomes more attenuated as mosquitoes become older. RNAi-based knockdown of eater, but not draper or
nimrod, decreased a mosquito's ability to kill Escherichia coli in the hemocoel. Knockdown of draper, eater, or any combination of
Nimrod family genes rendered mosquitoes more likely to die from Staphylococcus epidermidis. Finally, knockdown of
Nimrod family genes did not impact
mRNA levels of the
antimicrobial peptides defensin (def1),
cecropin (cecA) or gambicin (gam1), but eater knockdown led to a decrease in
mRNA levels of
nitric oxide synthase. Together, these data show that members of the A. gambiae
Nimrod gene family are positive regulators of the mosquito antibacterial response.