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. 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.
Interdisciplinary Research Centre, Justus-Liebig University, Giessen, Germany.
Kathrin
K
Buchholz
Stefan
S
Rahlfs
R Heiner
RH
Schirmer
Katja
K
Becker
Kai
K
Matuschewski
D000818:Animals; D001483:Base Sequence; D015153:Blotting, Western; D017931:DNA Primers; D008018:Life Cycle Stages; D010544:Peroxidases / Q000235:genetics*; D010962:Plasmodium berghei / Q000201:enzymology* / Q000254:growth & development; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D020133:Reverse Transcriptase Polymerase Chain Reaction
D017931:DNA Primers; D012333:RNA, Messenger; D010544:Peroxidases