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Mutant Parasites, Unable to Infect Hosts, Highlight Virulence Genes

and those that cause malaria, African sleeping sickness and water-borne diarrheal illnesses infect their hosts.

"This screen highlighted genes not previously seen as virulence factors," says Knoll. From one mutant, Knoll's team pinpointed a gene that acts as a nuclear traffic cop, directing molecular traffic in and out of the parasite's nucleus, where the DNA resides. Mutations in the gene, called RCC1 (Regulator of Chromosome Condensation 1), disrupt the flow of molecules, causing a trafficking breakdown that likely underlies the mutant parasite's inability to effectively sicken its host.

This study is the first evidence that this type of cellular function, called nuclear trafficking, may be important for infectivity, Knoll says.

"We hope to apply what we've learned here to other parasites," she says. "Our goal is to come up with new anti-parasitic drug targets." Currently, she says, there are few good treatments for most human parasitic infections, and even some of those are very toxic to patients.

RCC1 presents a promising potential target because the parasite versions of the gene are very different from human and other animal versions, which reduces the likelihood of toxic side effects.


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