Dataset Information

Sickle cell trait modulates the proteome and phosphoproteome of Plasmodium falciparum-infected erythrocyte

ABSTRACT: The high prevalence of sickle cell disease in some human populations likely results from the protection afforded against severe Plasmodium falciparum malaria and death by heterozygous carriage of HbS. P. falciparum remodels the erythrocyte membrane and skeleton, displaying parasite proteins at the erythrocyte surface that interact with key human proteins in the Ankyrin R and 4.1R complexes. Oxidative stress generated by HbS, as well as by parasite invasion, disrupts the kinase/phosphatase balance, potentially interfering with the molecular interactions between human and parasite proteins. HbS is known to be associated with abnormal membrane display of parasite antigens. Studying the proteome and the phosphoproteome of red cell membrane extracts from P. falciparum infected and non-infected erythrocytes, we show here that HbS heterozygous carriage, combined with infection, modulates the phosphorylation of erythrocyte membrane transporters and skeletal proteins as well as of parasite proteins. Our results highlight modifications of Ser- /Thr- and/or Tyr- phosphorylation in key human proteins, such as ankyrin, β-adducin, β-spectrin and Band 3, and key parasite proteins, such as RESA or MESA. Altered phosphorylation patterns could disturb the interactions within membrane protein complexes, affect nutrient uptake and the infected erythrocyte cytoadherence phenomenon, thus lessening the severity of malaria symptoms.

INSTRUMENT(S): Q Exactive Plus

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

TISSUE(S): Erythrocyte

SUBMITTER: Cerina Chhuon

LAB HEAD: Anaïs Merckx

PROVIDER: PXD023280 | Pride | 2021-04-19

REPOSITORIES: Pride

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			Action	DRS
	20180710_AnME_PAA1_P_1_7854.raw	Raw
	20180710_AnME_PAA1_P_2_7855.raw	Raw
	20180710_AnME_PAA1_P_3_7856.raw	Raw
	20180710_AnME_PAA2_P_1_7857.raw	Raw
	20180710_AnME_PAA2_P_2_7858.raw	Raw

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Publications

Sickle Cell Trait Modulates the Proteome and Phosphoproteome of Plasmodium falciparum-Infected Erythrocytes.

Chauvet Margaux M Chhuon Cerina C Lipecka Joanna J Dechavanne Sébastien S Dechavanne Célia C Lohezic Murielle M Ortalli Margherita M Pineau Damien D Ribeil Jean-Antoine JA Manceau Sandra S Le Van Kim Caroline C Luty Adrian J F AJF Migot-Nabias Florence F Azouzi Slim S Guerrera Ida Chiara IC Merckx Anaïs A

Frontiers in cellular and infection microbiology 20210324

The high prevalence of sickle cell disease in some human populations likely results from the protection afforded against severe Plasmodium falciparum malaria and death by heterozygous carriage of HbS. P. falciparum remodels the erythrocyte membrane and skeleton, displaying parasite proteins at the erythrocyte surface that interact with key human proteins in the Ankyrin R and 4.1R complexes. Oxidative stress generated by HbS, as well as by parasite invasion, disrupts the kinase/phos ...[more]

PMID: 33842387

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Project description:The pir genes comprise the largest multi-gene family in Plasmodium, with members found in P. vivax, P. knowlesi and the rodent malaria species. Despite comprising up to 5% of the parasite genome, little is known about the functions of the proteins encoded by pir genes. P. chabaudi causes chronic infection in mice, which may be due antigenic variation. In this model, pir genes are called cirs and may be involved in this mechanism allowing evasion of host immune responses. We have annotated the cir repertoire and performed detailed bioinformatic characterization of the encoded CIR proteins. Two major sub-families were identified: A and B, which display different amino acid motifs, and are thus predicted to have undergone functional divergence. The expression of all cirs was analyzed via RNA sequencing and microarray. Up to 40% of cir genes were expressed in the parasite population during infection, including members of both sub-families. Dominant cir transcripts could also be identified. Finally, specific cir genes were expressed at different time points during the blood stages of infection. Together our data characterizing the cir genes and their expression throughout the intra-erythrocytic cycle of development indicate that CIR proteins are likely to be important for parasite survival in the host. P. chabaudi AS is a highly synchronous parasite for which development in the blood follows its hostM-bM-^@M-^Ys circadian rhythm. Twelve time-points were then collected; one every two hours, to cover the entire 24 h cycle of blood stage development. At the peak of parasitaemia, one mouse was sacrificed at each time point and thin blood films were made and stained with Giemsa for optical microscopy. The pan-rodent microarray was designed using the OligoRankPick program as previously described: Liew, K et al.2010, Defining species specific genome differences in malaria parasites. BMC genomics 11,128. The RNA preparation, Cy-dye coupling to cDNA, hybridization and slide scanning were performed as described by Bozdech and colleagues Bozdech, Z et al 2003, The transcriptome of the intraerythrocytic developmental cycle of Plasmodium falciparum. PLoS Biol 1, E5.

Dataset Information

Sickle cell trait modulates the proteome and phosphoproteome of Plasmodium falciparum-infected erythrocyte

Dataset's files

Publications

Sickle Cell Trait Modulates the Proteome and Phosphoproteome of <i>Plasmodium falciparum</i>-Infected Erythrocytes.

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