Plasmodium falciparum GPCR-like receptor SR25 mediates extracellular K⁺ sensing coupled to Ca²⁺ signaling and stress survival.

ABSTRACT: 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 Ca²⁺ signaling in the parasites. Changing from high (140?mM) to low (5.4?mM) KCl concentration triggers [Ca²⁺]_cyt increase in isolated parasites and this Ca²⁺ rise is blocked either by phospholipase C (PLC) inhibition or by depleting the parasite's internal Ca²⁺ pools. This response persists even in the absence of free extracellular Ca²⁺ and cannot be elicited by addition of Na⁺, Mg²⁺ or Ca²⁺. However, when the PfSR25 gene was deleted, no effect on [Ca²⁺]_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.

SUBMITTER: Moraes MS 

PROVIDER: S-EPMC5573319 | biostudies-literature | 2017 Aug

REPOSITORIES: biostudies-literature