Depletion of Plasmodium berghei plasmoredoxin reveals a non-essential role for life cycle progression of the malaria parasite

Proliferation of the pathogenic Plasmodium asexual blood stages in host erythrocytes requires an exquisite capacity to protect the malaria parasite against oxidative stress. This function is achieved by a complex antioxidant defence system composed of redox-active proteins and low MW antioxidants. H...

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Published in:PloS one 2008-06, Vol.3 (6), p.e2474-e2474
Main Authors: Buchholz, Kathrin, Rahlfs, Stefan, Schirmer, R Heiner, Becker, Katja, Matuschewski, Kai
Format: Article
Language:English
Subjects:
Animals
Antigens
Antioxidants
Antioxidants (Nutrients)
Base Sequence
Biochemistry
Blotting, Western
Cell Biology/Microbial Growth and Development
Cell cycle
Chemical bonds
Deoxyribonucleic acid
Development and progression
DNA
DNA Primers
Drug development
E coli
Enzymes
Erythrocytes
Escherichia coli
Genes
Genetic aspects
Heat shock proteins
Infections
Infectious Diseases/Protozoal Infections
Interdisciplinary aspects
Life cycle analysis
Life cycle engineering
Life Cycle Stages
Life cycles
Malaria
Mathematical models
Microbiology/Cellular Microbiology and Pathogenesis
Microbiology/Parasitology
Mutants
Oxidative stress
Parasites
Parasitology
Peroxidases - genetics
Plasmodium
Plasmodium berghei
Plasmodium berghei - enzymology
Plasmodium berghei - growth & development
Plasmodium falciparum
Proteins
Rats
Reverse Transcriptase Polymerase Chain Reaction
Ribonucleotide reductase
RNA, Messenger - genetics
Rodents
Saccharomyces cerevisiae
Thioredoxin
Thioredoxins
Vector-borne diseases
Yeast
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description Proliferation of the pathogenic Plasmodium asexual blood stages in host erythrocytes requires an exquisite capacity to protect the malaria parasite against oxidative stress. This function is achieved by a complex antioxidant defence system composed of redox-active proteins and low MW antioxidants. Here, we disrupted the P. berghei plasmoredoxin gene that encodes a parasite-specific 22 kDa member of the thioredoxin superfamily. The successful generation of plasmoredoxin knockout mutants in the rodent model malaria parasite and phenotypic analysis during life cycle progression revealed a non-vital role in vivo. Our findings suggest that plasmoredoxin fulfils a specialized and dispensable role for Plasmodium and highlights the need for target validation to inform drug development strategies.
doi_str_mv 10.1371/journal.pone.0002474
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subjects Animals
Antigens
Antioxidants
Antioxidants (Nutrients)
Base Sequence
Biochemistry
Blotting, Western
Cell Biology/Microbial Growth and Development
Cell cycle
Chemical bonds
Deoxyribonucleic acid
Development and progression
DNA
DNA Primers
Drug development
E coli
Enzymes
Erythrocytes
Escherichia coli
Genes
Genetic aspects
Heat shock proteins
Infections
Infectious Diseases/Protozoal Infections
Interdisciplinary aspects
Life cycle analysis
Life cycle engineering
Life Cycle Stages
Life cycles
Malaria
Mathematical models
Microbiology/Cellular Microbiology and Pathogenesis
Microbiology/Parasitology
Mutants
Oxidative stress
Parasites
Parasitology
Peroxidases - genetics
Plasmodium
Plasmodium berghei
Plasmodium berghei - enzymology
Plasmodium berghei - growth & development
Plasmodium falciparum
Proteins
Rats
Reverse Transcriptase Polymerase Chain Reaction
Ribonucleotide reductase
RNA, Messenger - genetics
Rodents
Saccharomyces cerevisiae
Thioredoxin
Thioredoxins
Vector-borne diseases
Yeast
title Depletion of Plasmodium berghei plasmoredoxin reveals a non-essential role for life cycle progression of the malaria parasite
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