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Background  The recent reference genome assembly and annotation of the Asian malaria vector  Anopheles stephensi  detected only one gene encoding the leucine-rich repeat immune factor APL1, while in the  Anopheles gambiae  and sibling  Anopheles coluzzii , APL1 factors are encoded by a family of three paralogs. The phylogeny and biological function of the unique APL1 gene in  An. stephensi  have not yet been specifically examined.    Methods  The APL1 locus was manually annotated to confirm the computationally predicted single APL1 gene in  An. stephensi . APL1 evolution within  Anopheles  was explored by phylogenomic analysis. The single or paralogous APL1 genes were silenced in  An. stephensi  and  An. coluzzii , respectively, followed by mosquito survival analysis, experimental infection with  Plasmodium  and expression analysis.    Results  APL1 is present as a single ancestral gene in most  Anopheles  including  An. stephensi  but has expanded to three paralogs in an African lineage that includes only the  Anopheles gambiae  species complex and  Anopheles christyi . Silencing of the unique APL1 copy in  An. stephensi  results in significant mosquito mortality. Elevated mortality of APL1-depleted  An. stephensi  is rescued by antibiotic treatment, suggesting that pathology due to bacteria is the cause of mortality, and indicating that the unique APL1 gene is essential for host survival. Successful  Plasmodium  development in  An. stephensi  depends upon APL1 activity for protection from high host mortality due to bacteria. In contrast, silencing of all three APL1 paralogs in  An. coluzzii  does not result in elevated mortality, either with or without  Plasmodium  infection. Expression of the single  An. stephensi  APL1 gene is regulated by both the Imd and Toll immune pathways, while the two signaling pathways regulate different APL1 paralogs in the expanded APL1 locus.    Conclusions  APL1 underwent loss and gain of functions concomitant with expansion from a single ancestral gene to three paralogs in one lineage of African  Anopheles . We infer that activity of the unique APL1 gene promotes longevity in  An. stephensi  by conferring protection from or tolerance to an effect of bacterial pathology. The evolution of an expanded APL1 gene family could be a factor contributing to the exceptional levels of malaria transmission mediated by human-feeding members of the  An. gambiae  species complex in Africa.

Gene copy number and function of the APL1 immune factor changed during Anopheles evolution