摘要：The malaria parasite Plasmodium falciparum is exposed, during its development, to major changes of ionic composition in its surrounding medium. We demonstrate that the P. falciparum serpentine-like receptor PfSR25 is a monovalent cation sensor capable of modulating Ca(2+) signaling in the parasites. Changing from high (140 mM) to low (5.4 mM) KCl concentration triggers [Ca(2+)]cyt increase in isolated parasites and this Ca(2+) rise is blocked either by phospholipase C (PLC) inhibition or by depleting the parasite's internal Ca(2+) pools. This response persists even in the absence of free extracellular Ca(2+) and cannot be elicited by addition of Na(+), Mg(2+) or Ca(2+). However, when the PfSR25 gene was deleted, no effect on [Ca(2+)]cyt was observed in response to changing KCl concentration in the knocked out (PfSR25 (-)) parasite. Finally, we also demonstrate that: i) PfSR25 plays a role in parasite volume regulation, as hyperosmotic stress induces a significant decrease in parasite volume in wild type (wt), but not in PfSR25 (-) parasites; ii) parasites lacking PfSR25 show decreased parasitemia and metacaspase gene expression on exposure to the nitric oxide donor sodium nitroprusside (SNP) and iii), compared to PfSR25 (-) parasites, wt parasites showed a better survival in albumax-deprived condition.
