Molecular Biology and Microbiology professor Mark Muller has found that the protein, called MKRN1, promotes the destruction of an enzyme called telomerase that enables rapid duplication of cells. While researchers have known for years that healthy cells repress telomerase, they haven't understood why.
The work by Muller and In Kwong Chung and colleagues at Yonsei University in Seoul, South Korea, was published this month in Genes & Development.
The discovery is a big step that should generate excitement in the cancer research community, said Lee Johnson, chair of the Department of Molecular Genetics at the Ohio State University and an authority in gene expression in mammalian cells.
"To the best of my knowledge, this is the first example of how the enzyme (telomerase) itself can be turned off," Johnson said.
The work focuses on the role that a long stretch of repeated DNA known as a telomere has in influencing cell length and, in turn, its lifespan. Each of the human's 46 chromosomes is capped on either end by telomeres, which help protect the cells. Each time a cell divides, the telomeres are shortened until eventually they become so small that the cell stops multiplying. Eventually the cell is eliminated from the body.
When telomere ends do not shorten, division continues unabated. The body contains other mechanisms that kick in to stop the errant reproduction unless the telomerase enzyme is present. In laboratory tests, the MKRN1 protein has eliminated the presence of telomerase in tumor cells, said Muller, who conducted genetic research at The Ohio Sate University for 25 years before joining UCF last summer.
Muller said that the MKRN1 gene is incredibly ancient and has likely been part of a human genetic makeup since the begin
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Contact: Tom Evelyn
tevelyn@mail.ucf.edu
407-823-5988
University of Central Florida
19-Apr-2005