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Malaria is a worldwide health problem that affects two-thirds of the world population.  Plasmodium  invasion of anopheline mosquitoes is an obligatory step for malaria transmission. However, mosquito-malaria molecular interactions in nature are not clear. A genetic variation within mosquito fibrinogen related-protein 30 (FBN30) was previously identified to be associated with  Plasmodium falciparum  infection in natural  Anopheles gambiae  populations at malaria endemic areas in Kenya, and reducing FBN30 expression by RNAi makes mosquitoes more susceptible to  P. berghei . New results show that FBN30 is a secreted octamer that binds to both  P. berghei  and clinically circulating  P. falciparum  from malaria endemic areas in Kenya, but not laboratory  P. falciparum  strain NF54. Moreover, the natural genetic mutation (T to C) within FBN30 signal peptide, which changes the position 10 amino acid from phenylalanine to leucine, reduces protein expression by approximately half. This change is consistent to more susceptible  An. gambiae  to  P. falciparum  infection in the field. FBN30 in natural  An. gambiae  is proposed to work as a pathogen recognition molecule in inhibiting  P. falciparum  transmission in malaria endemic areas.

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FBN30 in wild Anopheles gambiae functions as a pathogen recognition molecule against clinically circulating Plasmodium falciparum in malaria endemic areas in Kenya