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

Miriam S. Moraes, Alexandre Budu, Maneesh K. Singh, Lucas Borges-Pereira, Julio Levano-Garcia, Chiara Currà, Leonardo Picci, Tomasino Pace, Marta Ponzi, Tullio Pozzan, Célia R.S. Garcia

Research output: Contribution to journalArticle

4 Citations (Scopus)

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.

Original languageEnglish
Article number9545
JournalScientific Reports
Volume7
Issue number1
DOIs
Publication statusPublished - Dec 1 2017

Fingerprint

Plasmodium falciparum
Parasites
Monovalent Cations
Parasitemia
Nitric Oxide Donors
Falciparum Malaria
Nitroprusside
Type C Phospholipases
Gene Expression

ASJC Scopus subject areas

  • General

Cite this

Moraes, M. S., Budu, A., Singh, M. K., Borges-Pereira, L., Levano-Garcia, J., Currà, C., ... Garcia, C. R. S. (2017). Plasmodium falciparum GPCR-like receptor SR25 mediates extracellular K+ sensing coupled to Ca2+ signaling and stress survival. Scientific Reports, 7(1), [9545]. https://doi.org/10.1038/s41598-017-09959-8

Plasmodium falciparum GPCR-like receptor SR25 mediates extracellular K+ sensing coupled to Ca2+ signaling and stress survival. / Moraes, Miriam S.; Budu, Alexandre; Singh, Maneesh K.; Borges-Pereira, Lucas; Levano-Garcia, Julio; Currà, Chiara; Picci, Leonardo; Pace, Tomasino; Ponzi, Marta; Pozzan, Tullio; Garcia, Célia R.S.

In: Scientific Reports, Vol. 7, No. 1, 9545, 01.12.2017.

Research output: Contribution to journalArticle

Moraes, Miriam S. ; Budu, Alexandre ; Singh, Maneesh K. ; Borges-Pereira, Lucas ; Levano-Garcia, Julio ; Currà, Chiara ; Picci, Leonardo ; Pace, Tomasino ; Ponzi, Marta ; Pozzan, Tullio ; Garcia, Célia R.S. / Plasmodium falciparum GPCR-like receptor SR25 mediates extracellular K+ sensing coupled to Ca2+ signaling and stress survival. In: Scientific Reports. 2017 ; Vol. 7, No. 1.
@article{fc58d0b345154c08a63a45861363bed3,
title = "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.",
author = "Moraes, {Miriam S.} and Alexandre Budu and Singh, {Maneesh K.} and Lucas Borges-Pereira and Julio Levano-Garcia and Chiara Curr{\`a} and Leonardo Picci and Tomasino Pace and Marta Ponzi and Tullio Pozzan and Garcia, {C{\'e}lia R.S.}",
year = "2017",
month = "12",
day = "1",
doi = "10.1038/s41598-017-09959-8",
language = "English",
volume = "7",
journal = "Scientific Reports",
issn = "2045-2322",
publisher = "Nature Publishing Group",
number = "1",

}

TY - JOUR

T1 - Plasmodium falciparum GPCR-like receptor SR25 mediates extracellular K+ sensing coupled to Ca2+ signaling and stress survival

AU - Moraes, Miriam S.

AU - Budu, Alexandre

AU - Singh, Maneesh K.

AU - Borges-Pereira, Lucas

AU - Levano-Garcia, Julio

AU - Currà, Chiara

AU - Picci, Leonardo

AU - Pace, Tomasino

AU - Ponzi, Marta

AU - Pozzan, Tullio

AU - Garcia, Célia R.S.

PY - 2017/12/1

Y1 - 2017/12/1

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=85028324719&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85028324719&partnerID=8YFLogxK

U2 - 10.1038/s41598-017-09959-8

DO - 10.1038/s41598-017-09959-8

M3 - Article

AN - SCOPUS:85028324719

VL - 7

JO - Scientific Reports

JF - Scientific Reports

SN - 2045-2322

IS - 1

M1 - 9545

ER -