The Mushroom's Secret Key
Researchers have identified a gene that allows the pathogenic yeast Candida albicans to attach to and invade intestinal cells. This discovery opens new perspectives for the treatments of fungal diseases. Candida albicans is normally a harmless inhabitant of the human gut, attaching itself to the walls of the human gut. However, when the immune system is weakened, the yeast sometimes develops long fibers and enters the bloodstream, causing infection and sometimes death. Deciphering the genetic control of this virulence has been quite complicated, as Candida regularly rearranges its large genome. In recent years, researchers have uncovered a number of genes that appear to control fiber growth, including a gene called INT1 that was cloned in the 1980s.
The protein encoded by INT1 resembles a group of structural proteins called integrins, which are involved in connecting cells to the extracellular matrix in vertebrates. Judith Berman and her colleagues from the University of Minnesota at St. Paul therefore suspected that INT1 could play an important role in the invasion of intestinal cells by the fungus. To test this hypothesis, they introduced INT1 into Saccharomyces cerevisiae, the harmless relative of Candida (Science 27 February 1998).
The mutated Saccharomyces promptly adhered to human cells in culture. Next, the researchers removed the INT1 gene from Candida and discovered that without the gene, Candida's ability to attach to human cells was greatly reduced, as was fiber growth. More important is the importance of the gene for the virulence of Candida: All mice injected with normal Candida died within 11 days, but 90% of mice injected with Candida lacking INT1 were 20 days post-injection still alive.
The results show that therapies targeting the INT1 protein may have an important role in the fight against Candida albicans infections.
