Knockdown of Anopheles dirus far upstream element‐binding protein gene lower oocyst numbers of Plasmodium vivax

Abstract

AbstractThe modulation of gene expression levels of Anopheles dirus on Plasmodium vivax infection at the ookinete and oocyst stages was previously reported. In the present study, several upregulated An. dirus genes were selected based on their high expression levels and subcellular locations to examine their roles in P. vivax infection. Five An. dirus genes—carboxylesterase, cuticular protein RR‐2 family, far upstream element‐binding protein, kraken, and peptidase212—were knocked down by dsRNA feeding using dsRNA‐lacZ as a control. The dsRNA‐fed mosquitoes were later challenged by P. vivax–infected blood, and the oocyst numbers were determined. The expression of these five genes was examined in many organs of both male and female mosquitoes. The results showed that the decreased expression level of the far upstream element‐binding protein gene could lower the oocyst numbers, whereas the others showed no effect on P. vivax infection. The expression levels of these genes in ovaries were found, and in many organs, they were similar between male and female mosquitoes. The reduction of these five gene expressions did not affect the lifespan of the mosquitoes. In addition, the malaria box compound, MMV000634, demonstrated the lowest binding energy to the far upstream element‐binding protein using virtual screening. This protein might be a target to block malaria transmission.