Dataset Information

Identification of STOML-interactors in the plasmodium mitochondrion

ABSTRACT: The STOML protein in plasmodium falciparum localizes in mitochondria in specific foci, at bbranching points and changes location during different stages of the parasite life cycle.

INSTRUMENT(S):

ORGANISM(S): Plasmodium Sp. F

TISSUE(S): Permanent Cell Line Cell, Cell Culture

DISEASE(S): Plasmodium Falciparum Malaria

SUBMITTER: Cornelia Spruijt

LAB HEAD: Taco W.A. Kooij

PROVIDER: PXD039772 | Pride | 2026-01-27

REPOSITORIES: Pride

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			Action	DRS
	20220803_Exploris1_SA_NS_EXT_JV_malaria_STOML_control_1.raw	Raw
	20220803_Exploris1_SA_NS_EXT_JV_malaria_STOML_control_2.raw	Raw
	20220803_Exploris1_SA_NS_EXT_JV_malaria_STOML_control_3.raw	Raw
	20220803_Exploris1_SA_NS_EXT_JV_malaria_STOML_mNEON_1.raw	Raw
	20220803_Exploris1_SA_NS_EXT_JV_malaria_STOML_mNEON_2.raw	Raw

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Project description:Drug resistance in Plasmodium falciparum remains a challenge for the malaria eradication programs around the world. With the emergence of artemisinin resistance, the efficacy of the partner drugs in the artemisinin combination therapies (ACT) that include quinoline based drugs is becoming critical. So far only few resistance markers have been identified and verified from which only two ABC transmembrane transporters namely PfMDR1 and PfCRT have been experimentally verified. Another P. falciparum ABC transporter, the multidrug resistance-associated protein (PfMRP2) represents an additional possible factor of drug resistance in P. falciparum. In this study, we identify a parasite clone that is derived from the 3D7 P. falciparum strain and which shows increased resistance to chloroquine and mefloquine through the trophozoite and schizont stages. We demonstrate that the resistance phenotype is caused by a 4.1 kb deletion in the 5M-bM-^@M-^Y upstream region of the pfmrp2 gene that leads to an alteration in the pfmrp2 transcription that result in increased levels of PfMRP2 protein. These results also suggest the importance of putative promoter elements in regulation of gene expression during the P. falciparum intra-erythrocytic developmental cycle and the potential of such genetic polymorphisms to underlie drug resistance phenotypes. Presented here are the data from microarray-based genome-wide transcriptomic and genomic studies of the drug-sensitive and drug-resistant 3D7 clones 11C/wt and 6A/mut. 2 P. falciparum lab clones derived from 3D7 strain were harvested during the intra-erythrocytic cycle for genomic DNA. gDNA were extracted by phenol chloroform. Synthesis of labelled target DNA was carried out as previously described: Bozdech, Z., M. Llinas, B. L. Pulliam, E. D. Wong, J. Zhu & J. L. DeRisi, (2003) The transcriptome of the intraerythrocytic developmental cycle of Plasmodium falciparum. PLoS Biol 1: E5, and used in comparative genomic microarray hybridizations (CGH).

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Identification of STOML-interactors in the plasmodium mitochondrion

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