RIVERSIDE, Calif. Malaria remains one of the most deadly infectious diseases. Yet, how Plasmodium, the malaria parasite, regulates its infectious cycle has remained an enigma despite decades of rigorous research.
But now a research team led by a cell biologist at the University of California, Riverside has identified a mechanism by which Plasmodium intensively replicates itself in human blood to spread the disease.
"If this mechanism can be stopped," said Karine Le Roch, an assistant professor of cell biology and neuroscience, who led the research, "Plasmodium replication would cease or be severely inhibited, thus controlling the spread of malaria."
In the cells of eukaryotes, such as the unicellular Plasmodium and humans, DNA, which can be as long as two meters, is closely packed to fit into the cell's tiny nucleus. Huge complex proteins called nucleosomes facilitate this DNA compaction so that eventually the DNA is coiled in an ordered manner to form chromosomes.
Made up of histone, a kind of protein, the nucleosomes are repeating units around which the double helix of DNA gets wrapped and vast amounts of genetic information get organized.
In trying to understand how the malaria parasite multiplies in red blood cells, Le Roch's team found that in Plasmodium a kind of "histone crash" takes place a massive breakdown of histone that explains how the parasite can replicate extensively its DNA and coding gene in human red blood cells.
For cell multiplication to occur, the genes in a DNA strand need to first be transcribed and translated (converted) into protein. For this transcription to take place, however, the nucleosomes must first get evicted (removed), a process that opens up the DNA strand to give special "transcription factors" full acce
|Contact: Iqbal Pittalwala|
University of California - Riverside