A 39-Amino-Acid C-Terminal Truncation of GDV1 Disrupts Sexual Commitment in Plasmodium falciparum

Author:

Tibúrcio Marta1,Hitz Eva23,Niederwieser Igor23,Kelly Gavin4,Davies Heledd1,Doerig Christian5,Billker Oliver67,Voss Till S.23ORCID,Treeck Moritz1ORCID

Affiliation:

1. Signalling in Apicomplexan Parasites Laboratory, The Francis Crick Institute, London, United Kingdom

2. Department of Medical Parasitology and Infection Biology, Swiss Tropical and Public Health Institute, Basel, Switzerland

3. University of Basel, Basel, Switzerland

4. Bioinformatics Science Technology Platform, The Francis Crick Institute, London, United Kingdom

5. Centre for Chronic Infectious and Inflammation Disease, Biomedical Sciences Cluster, School of Health and Biomedical Sciences, RMIT University, Bundoora, Australia

6. Billker Group, Rodent Models of Malaria, Wellcome Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridge, United Kingdom

7. Department of Molecular Biology and Molecular Infection Medicine Sweden, Umeå, Sweden

Abstract

Transmission of malaria-causing Plasmodium species by mosquitos requires the parasite to change from a continuously growing asexual parasite form growing in the blood to a sexually differentiated form, the gametocyte. Only a small subset of asexual parasites differentiates into gametocytes that are taken up by the mosquito.

Publisher

American Society for Microbiology

Subject

Molecular Biology,Microbiology

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