Dataset Information

TurboID Proximity Profiling of FIKK10.2 (PF3D7_1039000) in Plasmodium falciparum–Infected Red Blood Cells During Febrile Heat Stress

ABSTRACT: This project investigates how febrile heat stress alters the local protein environment of the Maurer’s cleft resident kinase FIKK10.2 in the malaria parasite Plasmodium falciparum. During human infection, parasites are routinely exposed to elevated temperatures associated with fever, yet how this physiological stress affects the organisation and trafficking of exported proteins within infected red blood cells remains poorly understood. To address this, we used proximity-dependent biotinylation (TurboID) to map changes in the protein neighbourhood of FIKK10.2 under normal and heat stress conditions. Transgenic parasites were generated expressing TurboID fused to the C-terminus of endogenous FIKK10.2. Highly synchronous (two hours window) asexual blood-stage parasites were exposed to febrile heat stress (39 °C) and compared with parasites maintained at standard culture temperature (37 °C). Biotin labelling was applied either continuously throughout the asexual life cycle or as a defined pulse between 16–24 hours post-invasion, with or without heat stress, resulting in three experimental conditions. Infected red blood cells were harvested at 40 hours post-invasion following Percoll density enrichment and lysed in 8 M urea. Proteins were digested to peptides, and biotinylated peptides were selectively enriched using anti-biotin antibodies. Enriched peptides were eluted under acidic conditions and analysed by liquid chromatography–tandem mass spectrometry. The resulting dataset provides a high-resolution view of the FIKK10.2 proximal proteome and, by extension, the Maurer’s cleft protein environment. These data reveal how febrile heat stress influences protein trafficking and local protein composition in P. falciparum, offering insights into temperature-dependent regulation of host cell remodelling during malaria infection.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human) Plasmodium Falciparum (isolate 3d7)

TISSUE(S): Blood Cell, Blood

DISEASE(S): Plasmodium Falciparum Malaria

SUBMITTER: David Jones

LAB HEAD: Moritz Treeck

PROVIDER: PXD073890 | Pride | 2026-05-14

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	DZ2362_20211025_biotin_full_rep1.raw	Raw
	DZ2362_20211025_biotin_full_rep2.raw	Raw
	DZ2362_20211025_biotin_full_rep3.raw	Raw
	DZ2362_20211025_biotin_pulse_heat_rep1.raw	Raw
	DZ2362_20211025_biotin_pulse_heat_rep2.raw	Raw

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Publications

Physiological febrile heat stress increases cytoadhesion through increased protein trafficking of <i>Plasmodium falciparum</i> surface proteins into the red blood cell.

Jones David D Belda Hugo H Broncel Malgorzata M Fuchs Gwendolin G Anaguano David D Nofal Stephanie D SD Treeck Moritz M

eLife 20260513

Fever is a hallmark of malaria. Several studies have linked febrile temperatures to reduced parasite viability, but also to increased cytoadhesion, a key driver of pathology. However, different mechanisms have been proposed to cause changes in cytoadhesion and parasite sensitivity to heat. Here, we demonstrate that exposure of <i>Plasmodium falciparum</i>-infected red blood cells (iRBCs) to physiologically relevant febrile heat stress (39 °C), derived from patient data, enhances cytoadhesion thr ...[more]

PMID: 42126964

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Project description:In eukaryotes, the chromatin architecture has a pivotal role in regulating all DNA-related processes. For P. falciparum, the causative agent of human malaria, the nucleosome landscape of the extremely AT-rich intergenic regulatory regions is largely unexplored. With the aid of a highly controlled MNase-seq procedure we reveal how positioning of nucleosomes provides a structural and regulatory framework to the transcriptional unit. We observe strong positioning of nucleosomes around splice sites that could aid co-transcriptional splicing events. In addition, nucleosome depleted regions are apparent hallmarks of transcription start sites (TSSs) and may support pre-initiation complex assembly. Moreover, we reveal nucleosome occupancy dynamics on strong TSSs during intraerythrocytic development, which correlate with gene expression changes and we observe a characteristic nucleosome architecture of functional - but not inert - TGCATGCA DNA motifs. Collectively, these findings highlight the regulatory capacity of the nucleosome landscape of this deadly human pathogen. Mnase-seq during the intra-erythrocytic asexual cycle of Plasmodium falciparum var2csa-panned 3D7 parasites for 8 time-points, every 5 hours starting from 5 hours post invasion until 40 hours post-invasion (T5-T40). Cycle length of these parasites is ~43 hours, synchronicity window is ~ 8 hours. T40 has 2 technical replicates (independent digestions; T40A, T40B). Additionally, pellet control sample (T15), histone H4-ChIP control (T40A) and sonicated and amplified genomic DNA. Chromatin was digested using a combined MNase + exonuclease III treatment. Libraries were prepared according to a Plasmodium-optimized library preparation procedure including KAPA polymerase-mediated PCR amplification. Strand-specific RNA-seq for expression quantification during the intra-erythrocytic asexual cycle of Plasmodium falciparum var2csa-panned 3D7 parasites for 8 time-points every 5 hours starting from 5 hours post invasion invasion until 40 hours post-invasion (T5-T40). Cycle length of these parasites is ~43 hours, synchronicity window is ~ 8 hours. These samples are originating from the exact same batch of parasites as are the MNase-Seq libraries. Libraries were prepared according to a Plasmodium-optimized library preparation procedure including KAPA polymerase-mediated PCR amplification.

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Dataset Information

TurboID Proximity Profiling of FIKK10.2 (PF3D7_1039000) in Plasmodium falciparum–Infected Red Blood Cells During Febrile Heat Stress

Dataset's files

Publications

Physiological febrile heat stress increases cytoadhesion through increased protein trafficking of <i>Plasmodium falciparum</i> surface proteins into the red blood cell.

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OmicsDI is part of the ELIXIR infrastructure

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Dataset Information

TurboID Proximity Profiling of FIKK10.2 (PF3D7_1039000) in Plasmodium falciparum–Infected Red Blood Cells During Febrile Heat Stress

Dataset's files

Publications

Physiological febrile heat stress increases cytoadhesion through increased protein trafficking of &lt;i&gt;Plasmodium falciparum&lt;/i&gt; surface proteins into the red blood cell.

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OmicsDI is part of the ELIXIR infrastructure

Tweets

Physiological febrile heat stress increases cytoadhesion through increased protein trafficking of <i>Plasmodium falciparum</i> surface proteins into the red blood cell.