Journal article

Knockdown of the translocon protein EXP2 in Plasmodium falciparum reduces growth and protein export

Sarah C Charnaud, Rasika Kumarasingha, Hayley E Bullen, Brendan S Crabb, Paul R Gilson



Malaria parasites remodel their host erythrocytes to gain nutrients and avoid the immune system. Host erythrocytes are modified by hundreds of effector proteins exported from the parasite into the host cell. Protein export is mediated by the PTEX translocon comprising five core components of which EXP2 is considered to form the putative pore that spans the vacuole membrane enveloping the parasite within its erythrocyte. To explore the function and importance of EXP2 for parasite survival in the asexual blood stage of Plasmodium falciparum we inducibly knocked down the expression of EXP2. Reduction in EXP2 expression strongly reduced parasite growth proportional to the degree of protein knock..

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Awarded by National Health and Medical Research Council of Australia

Funding Acknowledgements

These authors received the following grant funding from the National Health and Medical Research Council of Australia ( BSC and PRG [1068287 and 1128198] and BSC [1092789]. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.We thank the Australian Red Cross Blood Bank for the provision of human blood, Jacobus Pharmaceuticals for providing WR99210 and Monash Micro Imaging. We are grateful to Leann Tilley and Brian Cooke for providing ERC and SBP1 antibodies and Eva Pesce and Thorey Jonsdottir for technical assistance. The authors gratefully acknowledge funding from the Victorian Operational Infrastructure Support Program received by the Burnet Institute and for grants from the National Health and Medical Research Council of Australia (1068287, 1128198 and 1092789).