"We've observed that organisms may share many similar proteins and yet retain very little parallel function among them," said Taylor Sittler, a medical student at the University of Massachusetts Medical School in Worcester, Massachusetts. "For instance, Plasmodium falciparum--the parasite that causes malaria--shares with its human host many proteins involved in forming chromosomes during cell division, but those proteins may interact in different ways, creating different cellular pathways and even entirely different functions. This contradicts the currently accepted paradigm that shared proteins interact simply because their genes are conserved. It was quite unexpected," he added.
Malaria is the third leading cause of infectious disease death in the world, after tuberculosis and AIDS. The World Health Organization estimates the parasite causes acute illness in some 300 million people each year, resulting in about 2.7 million deaths.
Sittler, who conducted the research during his HHMI fellowship year at the University of California at San Diego (UCSD), is co-first author on a paper published in the November 3, 2005, issue of the journal Nature. The paper was co-authored by two UCSD colleagues, Silpa Suthram, a Ph.D. candidate in bioinformatics, and Trey Ideker, an assistant professor of bioengineering.
The team made the discovery while comparing protein networks of P. falciparum to protein networks in four model organisms: yeast, fruit flies, roundworms, and Helicobacter pylori, the bacteria that causes stomach ulcers. Their analysis drew on data developed by HHMI investigator Stanley Fields, a professor of genetics and yeast genome expert at the University of Washington
Contact: Jennifer Donovan
Howard Hughes Medical Institute