Julian's lab investigates the molecular details of human-parasite interactions during the P. falciparum blood stages, with a particular focus on genomic and proteomic approaches to understanding erythrocyte invasion.
Julian graduated from Lincoln University in New Zealand in 1993 with a degree in Biochemistry. He then moved to the UK to work as a graduate student in Dr Hugh Pelham's lab at the MRC Laboratory of Molecular Biology in Cambridge.
In Hugh's lab, Julian worked on membrane protein targeting in yeast and received his PhD from the University of Cambridge in 1998. While looking for a new research field to study as a post-doc, Julian stumbled across a review written by Dr John Barnwell describing how the major human malaria pathogen, Plasmodium falciparum, invades human erythrocytes. Erythrocyte invasion is a fascinating and still largely unexplained cell biological process that is an essential step in both parasite survival and malaria pathogenesis. Julian was hooked. From 1998 to 2002 he studied as a post-doctoral research fellow in John Barnwell's lab at the Centers for Disease Control and Prevention in Atlanta,where he helped identify and characterise a new family of P. falciparum ligands involved in erythrocyte recognition. In 2002, Julian became a faculty member in the Department of Medicine at the University of Alabama,Birmingham, where his team worked on the molecular details of how P. falciparum parasites recognise and invade human erythrocytes, and established strong links to field studies in the Peruvian Amazon.
Julian joined the Wellcome Trust Sanger Institute's Malaria Programme in 2008. The Sanger Intitute's Malaria Programme uses genomic and genetic approaches to discover molecular mechanisms of host-parasite interactions that may lead to new biological insights and improved strategies for disease prevention. Julian's lab investigates the molecular details of human-parasite interactions during the P. falciparum blood stages, with a particular focus on genomic and proteomic approaches to understanding erythrocyte invasion.
Malaria Programme: Rayner group
The Malaria Programme uses genomic and genetic approaches to discover molecular mechanisms of host-parasite interactions that may lead to new biological insights and improved strategies for disease prevention.
Plasmodium falciparum is the parasite responsible for the overwhelming majority of malaria mortality.
The Rayner group is investigating the molecular details of the interactions between P. falciparum and human red blood cells (erythrocytes), using both genomic and proteomic approaches.
The Rayner lab has a particular focus on erythrocyte invasion, the process by which P. falciparum parasites recognize and invade human red blood cells. This is a critical step in the parasite's life cycle, because once inside erythrocytes, P. falciparum parasites are protected from the antibody-mediated immune system, and use the hemoglobin within the blood cell to grow and multiply. By understanding erythrocyte invasion in depth, the Rayner group aims to identify molecular steps in the process that could be targeted by new drugs or vaccines.
An adaptable two-color flow cytometric assay to quantitate the invasion of erythrocytes by Plasmodium falciparum parasites.
Theron M, Hesketh RL, Subramanian S and Rayner JC
Cytometry Part A
Origin of the human malaria parasite Plasmodium falciparum in gorillas.
Liu W, Li Y, Learn GH, Rudicell RS, Robertson JD, Keele BF, Ndjango JB, Sanz CM, Morgan DB, Locatelli S, Gonder MK, Kranzusch PJ, Walsh PD, Delaporte E, Mpoudi-Ngole E, Georgiev AV, Muller MN, Shaw GM, Peeters M, Sharp PM, Rayner JC and Hahn BH
PUBMED: 20864995; PMC: 2997044; DOI: 10.1038/nature09442
Effects of calcium signaling on Plasmodium falciparum erythrocyte invasion and post-translational modification of gliding-associated protein 45 (PfGAP45).
Jones ML, Cottingham C and Rayner JC
Molecular and biochemical parasitology 2009;168;1;55-62
PUBMED: 19576251; PMC: 2754074; DOI: 10.1016/j.molbiopara.2009.06.007
Genetic diversity of the malaria vaccine candidate Plasmodium falciparum merozoite surface protein-3 in a hypoendemic transmission environment.
Jordan SJ, Branch OH, Castro JC, Castro JC, Oster RA and Rayner JC
The American journal of tropical medicine and hygiene 2009;80;3;479-86
PUBMED: 19270302; PMC: 2723947
Evolution of human-chimpanzee differences in malaria susceptibility: relationship to human genetic loss of N-glycolylneuraminic acid.
Martin MJ, Rayner JC, Gagneux P, Barnwell JW and Varki A
Proceedings of the National Academy of Sciences of the United States of America 2005;102;36;12819-24
PUBMED: 16126901; PMC: 1200275; DOI: 10.1073/pnas.0503819102
A Plasmodium falciparum homologue of Plasmodium vivax reticulocyte binding protein (PvRBP1) defines a trypsin-resistant erythrocyte invasion pathway.
Rayner JC, Vargas-Serrato E, Huber CS, Galinski MR and Barnwell JW
The Journal of experimental medicine 2001;194;11;1571-81
PUBMED: 11733572; PMC: 2193530