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Itoe, M.

Publications and source records attributed to Itoe, M..

2 recordsLinked to original sources

Additional blood meals increase mosquito infectivity by accelerating the transcriptional development of Plasmodium sporozoites

Sporozoites, the infectious stage of Plasmodium malaria parasites, must invade two different tissues in two very different hosts to ensure transmission: the mosquito salivary glands and the human liver. Whether infectivity to hepatocytes is affected by physiological components, such as the availability of nutrients within the Anopheles female, is not well understood. Here we show that Plasmodium falciparum sporozoite infectivity to hepatocytes is increased if mosquitoes take an additional blood meal while oocysts are developing. Infection rates of HC04.J7 hepatocytes at 24 h were 1.8-fold higher for P. falciparum salivary gland sporozoites isolated from Anopheles gambiae females fed twice (2BF) compared to those which only received the infectious blood meal (1BF). This increase in infectivity was observed at an early infection timepoint (day 11) and was accompanied by a marked shift in the transcriptional profiles of 2BF salivary gland sporozoites, identifying genes likely involved in infection and development in the mammalian host. Overall, our data reveal new factors potentially involved in sporozoite infectivity, and have broad implications for understanding transmission of malaria in endemic areas where multiple blood meals commonly shape available resources for adult female mosquitoes.

microbiology↗

Interplay between nutrient transporters ensures fertility in the malaria mosquito Anopheles gambiae

Females from many mosquito species feed on blood to acquire nutrients for egg development. The oogenetic cycle has been characterized in the arboviral vector Aedes aegypti, where after a bloodmeal, the lipid transporter lipophorin (Lp) shuttles lipids from the midgut and fat body to the ovaries, and a yolk precursor protein, vitellogenin (Vg), is deposited into the oocyte by receptor-mediated endocytosis. Our understanding of how the roles of these two nutrient transporters are mutually coordinated is however limited in this and other mosquito species. Here, we demonstrate that in the malaria mosquito Anopheles gambiae, Lp and Vg are reciprocally regulated in a timely manner to optimize egg development and ensure fertility. Defective lipid transport via Lp silencing triggers abortive ovarian follicle development, leading to misregulation of Vg and aberrant yolk granules. Conversely, depletion of Vg causes an upregulation of Lp in the fat body in a manner that appears to be at least partially dependent on target of rapamycin (TOR) signaling, resulting in excess lipid accumulation in the developing follicles. Embryos deposited by Vg-depleted mothers are completely infertile, and are arrested early during development, likely due to severely reduced amino acid levels and protein synthesis. Our findings demonstrate that the mutual regulation of these two nutrient transporters is essential to safeguard fertility by ensuring correct nutrient balance in the developing oocyte, and validate Vg and Lp as two potential candidates for mosquito control. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=127 SRC="FIGDIR/small/543516v1_ufig1.gif" ALT="Figure 1"> View larger version (42K): org.highwire.dtl.DTLVardef@1c9b326org.highwire.dtl.DTLVardef@1109e59org.highwire.dtl.DTLVardef@c263borg.highwire.dtl.DTLVardef@1a1f9df_HPS_FORMAT_FIGEXP M_FIG C_FIG

microbiology↗