ArticleBioMed research international2014
Role of calcium signaling in the transcriptional regulation of the apicoplast genome of Plasmodium falciparum.
Article in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Evolution of Resistance to Avian Malaria Infection in an Endemic Hawaiian Honeycreeper.Ecology and evolution · 2026Article
- In vitro delayed response to dihydroartemisinin of malaria parasites infecting sickle cell erythocytes.Malaria journal · 2024Article
- The Multistage Antimalarial Compound Calxinin PerturbatesPharmaceutics · 2022Article
- Machine Learning Uses Chemo-Transcriptomic Profiles to Stratify Antimalarial Compounds With Similar Mode of Action.Frontiers in cellular and infection microbiology · 2021Article
- The genetic CaThe Journal of biological chemistry · 2020Article
- Plasmodium falciparum apicoplast and its transcriptional regulation through calcium signaling.Journal of microbiology (Seoul, Korea) · 2017Review
- Potential Sabotage of Host Cell Physiology by Apicomplexan Parasites for Their Survival Benefits.Frontiers in immunology · 2017Review
- Modification of plant cell wall structure accompanied by enhancement of saccharification efficiency using a chemical, lasalocid sodium.Scientific reports · 2016Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Calcium is a universal second messenger that plays an important role in regulatory processes in eukaryotic cells. To understand calcium-dependent signaling in malaria parasites, we analyzed transcriptional responses of Plasmodium falciparum to two calcium ionophores (A23187 and ionomycin) that cause redistribution of intracellular calcium within the cytoplasm. While ionomycin induced a specific transcriptional response defined by up- or downregulation of a narrow set of genes, A23187 caused a developmental arrest in the schizont stage. In addition, we observed a dramatic decrease of mRNA levels of the transcripts encoded by the apicoplast genome during the exposure of P. falciparum to both calcium ionophores. Neither of the ionophores caused any disruptions to the DNA replication or the overall apicoplast morphology. This suggests that the mRNA downregulation reflects direct inhibition of the apicoplast gene transcription. Next, we identify a nuclear encoded protein with a calcium binding domain (EF-hand) that is localized to the apicoplast. Overexpression of this protein (termed PfACBP1) in P. falciparum cells mediates an increased resistance to the ionophores which suggests its role in calcium-dependent signaling within the apicoplast. Our data indicate that the P. falciparum apicoplast requires calcium-dependent signaling that involves a novel protein PfACBP1.
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