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Understanding the Development of Compensatory Pathways in a Mutant Malaria Parasite Harbouring Hypomorphic Allele of Plant-Like Kinases.
J Vis Exp
November 2024
Cellular and Molecular Parasitology Laboratory, School of Life Sciences, Jawaharlal Nehru University; Laboratory of Malaria and Vector Research and National Institutes of Allergy and Infectious Diseases, National Institutes of Health;
Article Synopsis
- The malaria parasite can alter its transcriptome to resist the effects of drugs, particularly affecting multigene families.
- CDPK family protein kinases in Plasmodium falciparum are crucial for its development and are potential targets for anti-malarial drugs.
- By using a chemical genetics approach to study a mutant parasite with a modified cdpk1 gene, researchers aim to discover compensatory mechanisms that could be targeted to combat drug resistance.
Mitochondrial ATP synthesis is essential for efficient gametogenesis in Plasmodium falciparum.
Commun Biol
November 2024
Department of Infection Biology, London School of Hygiene and Tropical Medicine, London, UK.
Plasmodium male and female gametocytes are the gatekeepers of human-to-mosquito transmission, therefore essential for propagation of malaria within a population. Whilst dormant in humans, their divergent roles during transmission become apparent soon after mosquito feeding with a rapid transformation into gametes - males forming eight motile sperm-like cells aiming to fertilise a single female gamete. Little is known about how the parasite fuels this abrupt change, and the potential role played by their large and elaborate cristate mitochondrion.
View Article and Find Full Text PDFIdentification of a divalent metal transporter required for cellular iron metabolism in malaria parasites.
Proc Natl Acad Sci U S A
November 2024
Department of Biochemistry, University of Utah School of Medicine, Salt Lake City, UT 84112.
malaria parasites invade and multiply inside red blood cells (RBCs), the most iron-rich compartment in humans. Like all cells, requires nutritional iron to support essential metabolic pathways, but the critical mechanisms of iron acquisition and trafficking during RBC infection have remained obscure. Parasites internalize and liberate massive amounts of heme during large-scale digestion of RBC hemoglobin within an acidic food vacuole (FV) but lack a heme oxygenase to release porphyrin-bound iron.
View Article and Find Full Text PDFIdentification of a divalent metal transporter required for cellular iron metabolism in malaria parasites.
bioRxiv
June 2024
Department of Biochemistry, University of Utah School of Medicine, Salt Lake City, UT, United States.
malaria parasites invade and multiply inside red blood cells (RBCs), the most iron-rich compartment in humans. Like all cells, requires nutritional iron to support essential metabolic pathways, but the critical mechanisms of iron acquisition and trafficking during RBC infection have remained obscure. Parasites internalize and liberate massive amounts of heme during large-scale digestion of RBC hemoglobin within an acidic food vacuole (FV) but lack a heme oxygenase to release porphyrin-bound iron.
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