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Background  We previously identified by genetic mapping an  Anopheles gambiae  chromosome region with strong influence over the outcome of malaria parasite infection in nature. Candidate gene studies in the genetic interval, including functional tests using the rodent malaria parasite  Plasmodium berghei , identified a novel leucine-rich repeat gene,  APL1 , with functional activity against  P. berghei .    Principal Findings  Manual reannotation now reveals  APL1  to be a family of at least 3 independently transcribed genes,  APL1A ,  APL1B , and  APL1C . Functional dissection indicates that among the three known  APL1  family members,  APL1C  alone is responsible for host defense against  P. berghei . APL1C functions within the Rel1-Cactus immune signaling pathway, which regulates  APL1C  transcript and protein abundance. Gene silencing of  APL1C  completely abolishes Rel1-mediated host protection against  P. berghei , and thus the presence of APL1C is required for this protection. Further highlighting the influence of this chromosome region, allelic haplotypes at the APL1 locus are genetically associated with and have high explanatory power for the success or failure of  P. berghei  parasite infection.    Conclusions    APL1C  functions as a required transducer of Rel1-dependent immune signal(s) to efficiently protect mosquitoes from  P. berghei  infection, and allelic genetic haplotypes of the  APL1  locus display distinct levels of susceptibility and resistance to  P. berghei .

Anopheles gambiae APL1 Is a Family of Variable LRR Proteins Required for Rel1-Mediated Protection from the Malaria Parasite, Plasmodium berghei