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1.
Int J Mol Sci ; 22(1)2021 Jan 05.
Article in English | MEDLINE | ID: mdl-33466510

ABSTRACT

Ca2+ signaling has been involved in controling critical cellular functions such as activation of proteases, cell death, and cell cycle control. The endoplasmatic reticulum plays a significant role in Ca2+ storage inside the cell, but mitochondria have long been recognized as a fundamental Ca2+ pool. Protozoan parasites such as Plasmodium falciparum, Toxoplasma gondii, and Trypanosoma cruzi display a Ca2+ signaling toolkit with similarities to higher eukaryotes, including the participation of mitochondria in Ca2+-dependent signaling events. This review summarizes the most recent knowledge in mitochondrial Ca2+ signaling in protozoan parasites, focusing on the mechanism involved in mitochondrial Ca2+ uptake by pathogenic protists.


Subject(s)
Calcium Signaling/physiology , Calcium/metabolism , Mitochondria/metabolism , Parasites/metabolism , Animals , Eukaryota/metabolism , Humans , Plasmodium falciparum/metabolism , Protozoan Proteins/metabolism , Toxoplasma/metabolism , Trypanosoma cruzi/metabolism
2.
J Pineal Res ; 66(2): e12484, 2019 03.
Article in English | MEDLINE | ID: mdl-29480948

ABSTRACT

Malaria causes millions of deaths worldwide and is considered a huge burden to underdeveloped countries. The number of cases with resistance to all antimalarials is continuously increasing, making the identification of novel drugs a very urgent necessity. A potentially very interesting target for novel therapeutic intervention is the parasite mitochondrion. In this work, we studied in Plasmodium falciparum 3 genes coding for proteins homologues of the mammalian FIS1 (Mitochondrial Fission Protein 1) and DRP1 (Dynamin Related Protein 1) involved in mitochondrial fission. We studied the expression of P. falciparum genes that show ample sequence and structural homologies with the mammalian counterparts, namely FIS1, DYN1, and DYN2. The encoded proteins are characterized by a distinct pattern of expression throughout the erythrocytic cycle of P. falciparum, and their mRNAs are modulated by treating the parasite with the host hormone melatonin. We have previously reported that the knockout of the Plasmodium gene that codes for protein kinase 7 is essential for melatonin sensing. We here show that PfPk7 knockout results in major alterations of mitochondrial fission genes expression when compared to wild-type parasites, and no change in fission proteins expression upon treatment with the host hormone. Finally, we have compared the morphological characteristics (using MitoTracker Red CMX Ros) and oxygen consumption properties of P. falciparum mitochondria in wild-type parasites and PfPk7 Knockout strains. A novel GFP construct targeted to the mitochondrial matrix to wild-type parasites was also developed to visualize P. falciparum mitochondria. We here show that, the functional characteristics of P. falciparum are profoundly altered in cells lacking protein kinase 7, suggesting that this enzyme plays a major role in the control of mitochondrial morphogenesis and maturation during the intra-erythrocyte cell cycle progression.


Subject(s)
Genes, Protozoan/drug effects , Melatonin/pharmacology , Mitochondrial Dynamics/drug effects , Mitochondrial Dynamics/physiology , Plasmodium falciparum/metabolism , Dynamins/metabolism , Erythrocytes/parasitology , Gene Knockout Techniques , Green Fluorescent Proteins , Humans , Mitochondria/drug effects , Mitochondrial Proteins/metabolism , Plasmodium falciparum/drug effects , Protein Kinases/metabolism
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