Malaria is one of the most devastating diseases worldwide causing over 1.5 million deaths and afflicting over 300 million people annually, mostly children. This disease is caused by apicomplexan parasites of the genus Plasmodium. There are four species of Plasmodium that affect humans and transmission from person to person occurs through the female Anopheles mosquito. While the past century has seen significant progress in anti-malarial drug development, many of these drugs are currently losing their efficacy due to the rise of drug resistant Plasmodium strains. The challenge we face is to identify and characterize novel targets for anti-malarial strategies.
Our lab works on the deadliest form of the parasite, Plasmodium falciparum. The lifecycle of P. falciparum is incredibly diverse and involves complex developmental stages in three vastly different hosts: the mosquito, the human liver, and human red blood cells. The developmental progression of the parasite through these stages is, in part, controlled through regulation of gene expression. We have found that there is a cascade of gene expression during the red blood cell stage of development with most genes expressed in a highly periodic manner. While at many levels, regulation of gene expression in P. falciparum resembles that of other eukaryotes, there are unique features, which indicate that regulation may be quite unique.
Research in our laboratory is focused on understanding the mechanisms of gene regulation in Plasmodium. We plan to capitalize on the unique features of Plasmodium gene regulation to design ways to disrupt parasite development and ultimately contribute to a cure for malaria. To dissect these mechanisms we are applying functional genomics approaches incorporating bioinformatics, whole-genome technologies, biochemistry, and molecular biology.