Complement-like protein TEP1 is a determinant of vectorial capacity in the malaria vector Anopheles gambiae.
Anopheles mosquitoes are major vectors of human malaria in Africa. Large variation exists in the ability of mosquitoes to serve as vectors and to transmit malaria parasites, but the molecular mechanisms that determine vectorial capacity remain poorly understood. We report that the hemocyte-specific complement-like protein TEP1 from the mosquito Anopheles gambiae binds to and mediates killing of midgut stages of the rodent malaria parasite Plasmodium berghei. The dsRNA knockdown of TEP1 in adults completely abolishes melanotic refractoriness in a genetically selected refractory strain. Moreover, in susceptible mosquitoes this knockdown increases the number of developing parasites. Our results suggest that the TEP1-dependent parasite killing is followed by a TEP1-independent clearance of dead parasites by lysis and/or melanization. Further elucidation of the molecular mechanisms of TEP1-mediated parasite killing will be of great importance for our understanding of the principles of vectorial capacity in insects.
European Molecular Biology Laboratory, Meyerhofstrasse 1, 69117 Heidelberg, Germany.
Stephanie
S
Blandin
Shin-Hong
SH
Shiao
Luis F
LF
Moita
Chris J
CJ
Janse
Andrew P
AP
Waters
Fotis C
FC
Kafatos
Elena A
EA
Levashina
D000595:Amino Acid Sequence; D000818:Animals; D000852:Anopheles / Q000033:anatomy & histology / Q000378:metabolism* / Q000469:parasitology*; D005260:Female; D006801:Humans; D019476:Insect Proteins / Q000737:chemistry / Q000235:genetics / Q000378:metabolism*; D007303:Insect Vectors / Q000235:genetics / Q000469:parasitology / Q000502:physiology*; D008288:Malaria / Q000453:epidemiology*; D008958:Models, Molecular; D008969:Molecular Sequence Data; D010962:Plasmodium berghei / Q000166:cytology / Q000502:physiology; D011110:Polymorphism, Genetic; D017434:Protein Structure, Tertiary; D012313:RNA / Q000378:metabolism; D016415:Sequence Alignment
D019476:Insect Proteins; D012313:RNA