Effect of Plasmodium yoelii nigeriensis (Haemosporidia: Plasmodiidae) on Anopheles stephensi (Diptera: Culicidae) vitellogenesis.
Our previous studies demonstrated a significant reduction in the egg production and survival of Anopeles stephensi Liston infected with Plasmodium yoelii nigeriensis Killick-Kendrick. We investigated the physiological mechanism underlying the malaria-induced curtailment of reproductive fitness. Polyclonal antibodies were raised against An. stephensi vitellin (Vn) and used in an enzyme immunoassay to quantify ovarian Vn and hemolymph vitellogenin (Vg) at 8, 12, 16, 20, 24, and 48 h postblood feeding in infected and noninfected mosquitoes. Initially, the concentration of Vg in the hemolymph and the accumulation of Vn in the ovaries of infected females were identical to females fed on noninfected mice, indicating that the synthesis of yolk protein by the fat bodies was initiated normally. However, there was a significant reduction in ovarian Vn at 24 and 48 h postblood feeding and a significant accumulation of Vg at 20 and 24 h postblood feeding in the hemolymph of infected mosquitoes. This increase in concentration of Vg in the hemolymph just before Vn reduction in the ovaries of infected mosquitoes indicated that synthesis at the fat body level may not be affected, but that sequestration of Vg by ovarian follicles of malaria-infected mosquitoes may be affected before resorbing follicles lose protein.
Jahan
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Department of Biological Sciences, Keele University, Staffordshire, UK.
Hurd
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D000818:Animals; D000852:Anopheles / Q000469:parasitology* / Q000502:physiology*; D005260:Female; D006458:Hemolymph / Q000502:physiology; D006790:Host-Parasite Interactions / Q000502:physiology; D051379:Mice; D010053:Ovary / Q000502:physiology; D010058:Oviposition; D010961:Plasmodium / Q000502:physiology*; D012098:Reproduction / Q000502:physiology*; D014818:Vitellogenesis / Q000502:physiology*; D014819:Vitellogenins / Q000032:analysis
D014819:Vitellogenins