Researchers receive NIH grant to study 3-D structure of Plasmodium's genome during parasite's erythrocytic cycle

Jun 28 2013

Malaria is one of the most important infectious diseases in the developing world, with the absence of a vaccine and the development of parasite resistance to commonly used antimalarial drugs complicating efforts to fight the deadly disease.

The parasite that causes malaria is Plasmodium, which requires specific human and mosquito tissues to complete its life cycle. The progression and control of this life cycle could be better understood by studying changes of the 3-D structure of the parasite's genome.

The University of California, Riverside and the University of Washington have received a four-year grant of more than $2 million from the National Institutes of Health to discover this 3-D structure of Plasmodium's genome during the parasite's erythrocytic cycle that is responsible for disease in humans.

The erythrocytic cycle that the researchers will study is a 48-hour cycle that can repeat for several days or weeks in humans.

Karine Le Roch, an associate professor of cell biology and neuroscience, is the principal investigator of the grant to UC Riverside. Her lab will work closely with the lab of William Stafford Noble, a professor of genome sciences at the University of Washington. Approximately $1 million of the total funding will be allocated to UCR.

"There are a few publications on the 3-D structure of the yeast and human genomes under particular conditions, but no one has so far analyzed the 3-D structure of a genome's organism during its cell cycle progression," Le Roch said.

The researchers will use the resulting 3-D structure data from their work in combination with new genome-wide data sets to develop a computational three-dimensional model that they expect will yield insights into how parasite genes are regulated.

"Rational drug design requires a detailed understanding of the molecular basis of disease," Le Roch said. "By providing fundamental insight into the regulatory mechanisms of Plasmodium, this project will improve our ability to design new drugs and novel lines of defense against malaria."

Source: University of California - Riverside