Has anyone not seen those TV pharmaceutical commercials with attractive 30-something women discussing their yeast infections? The culprits of these hushed conversations-and of 10 percent of hospital infections-are Candida yeasts. Molecular biologist Brendan Cormack is trying to unravel the mechanisms through which Candida yeast causes infections. To be precise, he's trying to pinpoint the few genes that allow Candida to trigger disease, while all over the world people happily ingest one of Candida's close cousins, baker's yeast (Saccharomyces cerevisae), in their staffs of life, bread and wine. To gather their information, the Cormack group is studying one specific species of Candida, called Candida glabrata. In fact, they've created 20,000 different versions of Candida glabrata. Their plan is to identify the few mutants among these that are not infectious and thereby gain insight into how the infection process works. The lab group already has identified one gene, the EPA1 gene (for epithelial adhesion 1), as an important player. The protein produced by the EPA1 gene, it seems, helps the yeast bind to human cells, a step crucial for infection. By searching through all the genes in Candida glabrata, the Cormack group has discovered that the EPA1 gene is surrounded by other genes closely related to it that also may be involved in the critical binding step of infection. What's more, Cormack has found that EPA1 and its neighbors are physically located in a region generally reserved for those genes that allow the cell to survive in different environments (like the human host). Eventually, what the group has learned about adherence could prove critical in designing drugs that target the proteins involved in this early step in the infection process. One thing seems certain: if the lab succeeds in exposing the workings of Candida glabrata, pharmaceutical companies will be beating a path to their door. Hopkins Medical News
Fall 2002 | 
