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.
%0 Journal Article
%1 Buchholz.2008
%A Buchholz, Kathrin
%A Rahlfs, Stefan
%A Schirmer, Heiner R.
%A Becker, Katja
%A Matuschewski, Kai
%D 2008
%J PLoS ONE
%K Animals Base_Sequence Blotting DNA_Primers IFZ Life_Cycle_Stages Messenger Peroxidases Plasmodium_berghei RNA Rats Reverse_Transcriptase_Polymerase_Chain_Reaction Western
%N 6
%P e2474-e2474
%T Depletion of Plasmodium berghei plasmoredoxin reveals a non-essential role for life cycle progression of the malaria parasite
%V 3
%X 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.
@article{Buchholz.2008,
abstract = {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.},
added-at = {2008-10-14T16:07:18.000+0200},
author = {Buchholz, Kathrin and Rahlfs, Stefan and Schirmer, Heiner R. and Becker, Katja and Matuschewski, Kai},
biburl = {https://www.bibsonomy.org/bibtex/288be58900ce4b5c3072293d9fbc91bf8/nutribiochem},
interhash = {872707ee175822f4914a1a0af2d30325},
intrahash = {88be58900ce4b5c3072293d9fbc91bf8},
issn = {1932-6203},
journal = {PLoS ONE},
keywords = {Animals Base_Sequence Blotting DNA_Primers IFZ Life_Cycle_Stages Messenger Peroxidases Plasmodium_berghei RNA Rats Reverse_Transcriptase_Polymerase_Chain_Reaction Western},
number = 6,
pages = {e2474-e2474},
timestamp = {2008-10-14T16:08:41.000+0200},
title = {Depletion of Plasmodium berghei plasmoredoxin reveals a non-essential role for life cycle progression of the malaria parasite},
volume = 3,
year = 2008
}