Open Accessclag9 : A cytoadherence gene in Plasmodium falciparum essential for binding of parasitized erythrocytes to CD36
Author(s) -
Katharine R. Trenholme,
Donald L. Gardiner,
Deborah C. Holt,
Elizabeth A. Thomas,
Alan F. Cowman,
David J. Kemp
Publication year - 2000
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.040561197
Subject(s) - plasmodium falciparum , biology , gene , cd36 , clone (java method) , transmembrane protein , gene family , microbiology and biotechnology , genetics , gene product , chromosome , gene expression , malaria , immunology , receptor
The propensity of isolates of the malaria parasitePlasmodium falciparum to delete a segment of chromosome 9 has provided positional information that has allowed us to identify a gene necessary for cytoadherence. It has been termed the cytoadherence-linked asexual gene (clag9 ).clag9 encodes at least nine exons and is expressed in blood stages. The hydrophobicity profile of the predicted CLAG9 protein identifies up to four transmembrane domains. We show here that targeted gene disruption ofclag 9 ablated cytoadherence to C32 melanoma cells and purified CD36. DNA-induced antibodies to theclag9 gene product reacted with a polypeptide of 220 kDa in the parental malaria clone but not in clones with a disruptedclag9 gene.