New antiparasitic agents are needed for severe malaria due to the protozoan pathogen, Plasmodium falciparum. We believe that improving our fundamental understanding of the basic molecular and cellular biology of this organism is key to finding new drug targets against the parasite.

 

Our lab focuses on the deoxyxylulose phosphate (DXP) non-mevalonate pathway of isoprenoid biosynthesis in P. falciparum, which is likely essential for parasite growth. Isoprenoids are a very diverse class of biomolecules with numerous functions within the cell, including co-factors, electron transport, and signaling molecules.  The Odom lab studies the developmental effects of isoprenoid blockade, and is working to understand why isoprenoids are important to Plasmodia development. The parasite DXP pathway is biochemically distinct from the mevalonate pathway in humans, making it a particularly interesting drug target.

 

Despite the complexity of the malaria life cycle, little is understood about the fundamental molecular signals that drive parasite development. Genome sequencing efforts of P. falciparum and related organisms have revealed a relative paucity of classical mammalian signaling players: for example, there are no clear tyrosine kinase or IP₃-receptor homologues. It seems likely that P. falciparum will use a limited number of signals in a novel way, or there may be additional signaling pathways that remain as yet identified. Additional projects in the Odom lab address the role of those signaling pathways that do appear to be intact in Plasmodia.

 

Our lab is part of the Pathobiology Research Unit in the Department of Pediatrics. It is located on the 6th floor of the McDonnell Pediatric Research Building.

 

 

Left, EM of malaria trophozoite; Right, Multinucleated malaria schizont

 

New antiparasitic agents are needed for severe malaria due to the protozoan pathogen, Plasmodium falciparum. We believe that improving our fundamental understanding of the basic molecular and cellular biology of this organism is key to finding new drug targets against the parasite.

 

Our lab focuses on the deoxyxylulose phosphate (DXP) non-mevalonate pathway of isoprenoid biosynthesis in P. falciparum, which is likely essential for parasite growth. Isoprenoids are a very diverse class of biomolecules with numerous functions within the cell, including co-factors, electron transport, and signaling molecules.  The Odom lab studies the developmental effects of isoprenoid blockade, and is working to understand why isoprenoids are important to Plasmodia development. The parasite DXP pathway is biochemically distinct from the mevalonate pathway in humans, making it a particularly interesting drug target.

 

Despite the complexity of the malaria life cycle, little is understood about the fundamental molecular signals that drive parasite development. Genome sequencing efforts of P. falciparum and related organisms have revealed a relative paucity of classical mammalian signaling players: for example, there are no clear tyrosine kinase or IP₃-receptor homologues. It seems likely that P. falciparum will use a limited number of signals in a novel way, or there may be additional signaling pathways that remain as yet identified. Additional projects in the Odom lab address the role of those signaling pathways that do appear to be intact in Plasmodia.

 

Our lab is part of the Pathobiology Research Unit in the Department of Pediatrics. It is located on the 6th floor of the McDonnell Pediatric Research Building.

 

 

Left, EM of malaria trophozoite; Right, Multinucleated malaria schizont