The endoplasmic reticulum-resident serpentine receptor SR10 has important functions for asexual and sexual blood stage development of Plasmodium falciparum

https://doi.org/10.1016/j.molbiopara.2020.111315Get rights and content

Highlights

  • The genome of Plasmodium falciparum encodes the serpentine receptor SR10.

  • SR10 is expressed in the asexual and sexual blood stages of P. falciparum.

  • SR10 associates with the endoplasmic reticulum of the P. falciparum blood stages.

  • Loss of SR10 impairs intraerythrocytic replication and gametocyte development.

Abstract

Serpentine receptors (SRs) are transmembrane proteins generally acting as mediators to facilitate the communication between a cell and its environment. At least six putative SR-like proteins are encoded in the genome of the malaria parasite Plasmodium falciparum. For two of them, roles in cell stress control were reported; however, for most of the SR-like proteins the functions are not yet known. In this study, we provide a first phenotypic analysis of the plasmodial SR10. The transmembrane protein is expressed in the asexual and sexual blood stages of P. falciparum. Co-localization and co-immunoprecipitation assays demonstrated an association of SR10 with the endoplasmic reticulum protein ERC. Gene disruption of SR10 leads to impaired intraerythrocytic replication and strongly reduces gametocyte numbers. We thus propose that SR10 is a protein associated with the endoplasmic reticulum that has important functions for asexual and sexual blood stage development.

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CRediT authorship contribution statement

Emilie Joëlle Njila Tchoufack: Methodology, Writing - original draft. Lena Hahnfeld: Validation. Georg Pitschelatow: Methodology. Sandra Bennink: Writing - review & editing, Validation. Gabriele Pradel: Conceptualization, Writing - review & editing.

Declaration of Competing Interest

The authors have no conflict of interest to declare.

Acknowledgement

The authors thank Tobias Spielmann (BNITM Hamburg) for providing the pSLI-TGD vector and Che Julius Ngwa (RWTH Aachen University) for critically reading the manuscript. EJNT was funded by a PhD fellowship from the German Academic Exchange Service (DAAD).

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