Quantitative protein expression profiling reveals extensive post-transcriptional regulation and post-translational modifications in schizont-stage malaria parasites

Bernardo J Foth,Neng Zhang,Zbynek Bozdech,Peter R Preiser,Sachel Mok

doi:10.1186/gb-2008-9-12-r177

Bernardo J Foth, Neng Zhang + Show 3 more

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https://doi.org/10.1186/gb-2008-9-12-r177

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Journal: Genome Biology	Publication Date: Jan 1, 2008
Citations: 183	License type: cc-by

Affiliation: Nanyang Technological University

Abstract

A quantitative time-course analysis of protein abundance for Plasmodium falciparum schizonts using two-dimensional differential gel electrophoresis reveals significant post-transcriptional regulation.

Highlights

Malaria is a one of the most important infectious diseases and is caused by parasitic protozoa of the genus Plasmodium
In this study we used two-dimensional differential gel electrophoresis (2D-DIGE) [32] in quantitative proteomics analyses to investigate the extent of post-transcriptional gene regulation and posttranslational modifications (PTMs) during the late section of the P. falciparum intra-erythrocytic developmental cycle (IDC). We demonstrate that this technique provides high reproducibility suitable for quantitative measurements of relative protein abundance from samples collected at short time intervals from a highly synchronous P. falciparum culture
Each individual time point (TP) protein preparation was run in four separate experiments utilizing first-dimension strips spanning pH 3 to pH 7

Summary

Introduction

Quantitative characterization of the P. falciparum transcriptome demonstrated that the strictly controlled progression of these parasites through their intra-erythrocytic developmental cycle is accompanied by a continuous cascade of gene expression. After the injection of infectious sporozoites into the human host and an initial round of hepatocyte infection, the parasites replicate within red blood cells, progressing through an intra-erythrocytic developmental cycle (IDC) that takes the parasites about 48 hours to complete. Daughter cells are produced within the schizonts (about 32 to 48 HPI), with the release of multiple free merozoites marking the end of the IDC This rapid asexual multiplication during the Plasmodium IDC causes the trademark clinical symptoms of the disease, ranging from fever, muscle aches and anemia, to organ failure, coma and death. The abundance of the blood-stage parasites and their prolonged occurrence in the human host render the IDC an important target of available antimalaria chemotherapies, as well as new drug-based and vaccine-based intervention strategies that are being developed

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