Instituto de Medicina Molecular, Faculdade de Medicina da Universidade de Lisboa, Edifício Egas Moniz, Av. Prof. Egas Moniz, Lisbon, Portugal
Saskia Egarter
Parasitology, Department of Infectious Diseases, University of Heidelberg Medical School, Heidelberg, Germany
Vanessa Zuzarte-Luís
Instituto de Medicina Molecular, Faculdade de Medicina da Universidade de Lisboa, Edifício Egas Moniz, Av. Prof. Egas Moniz, Lisbon, Portugal
Hirdesh Kumar
Parasitology, Department of Infectious Diseases, University of Heidelberg Medical School, Heidelberg, Germany; Kusuma School of Biological Sciences, Indian Institute of Technology Delhi, New Delhi, India
Catherine A Moreau
Parasitology, Department of Infectious Diseases, University of Heidelberg Medical School, Heidelberg, Germany
Instituto de Medicina Molecular, Faculdade de Medicina da Universidade de Lisboa, Edifício Egas Moniz, Av. Prof. Egas Moniz, Lisbon, Portugal; Parasitology, Department of Infectious Diseases, University of Heidelberg Medical School, Heidelberg, Germany
Gliding motility allows malaria parasites to migrate and invade tissues and cells in different hosts. It requires parasite surface proteins to provide attachment to host cells and extracellular matrices. Here, we identify the Plasmodium protein LIMP (the name refers to a gliding phenotype in the sporozoite arising from epitope tagging of the endogenous protein) as a key regulator for adhesion during gliding motility in the rodent malaria model P. berghei. Transcribed in gametocytes, LIMP is translated in the ookinete from maternal mRNA, and later in the sporozoite. The absence of LIMP reduces initial mosquito infection by 50%, impedes salivary gland invasion 10-fold, and causes a complete absence of liver invasion as mutants fail to attach to host cells. GFP tagging of LIMP caused a limping defect during movement with reduced speed and transient curvature changes of the parasite. LIMP is an essential motility and invasion factor necessary for malaria transmission.
