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

PLoS One. 2008 Jun 25;3(6):e2474. doi: 10.1371/journal.pone.0002474.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Base Sequence
  • Blotting, Western
  • DNA Primers
  • Life Cycle Stages
  • Peroxidases / genetics*
  • Plasmodium berghei / enzymology*
  • Plasmodium berghei / growth & development
  • RNA, Messenger / genetics
  • Rats
  • Reverse Transcriptase Polymerase Chain Reaction


  • DNA Primers
  • RNA, Messenger
  • Peroxidases