The end portions of chromosomes, called telomeres, contain repeating sequences of DNA that protect the chromosomes from damage, said Toru Nakamura, a CU-Boulder researcher, Howard Hughes Medical Institute scientist and lead author on the study. Since portions of the telomeres are lost each time a cell divides, telomere shortening is thought to act as a molecular clock of sorts by signaling the cell to stop dividing after repeated cell divisions.
But the telomerase enzyme counteracts telomere shortening by adding DNA back onto the chromosome ends, he said. Normal cells do not contain telomerase, and their telomeres shorten with each cell division until they stop dividing. In cancer cells, however, telomerase is thought to grant the cell immortality by maintaining telomere length so that the cell never receives a signal to stop dividing.
"Correlation of telomerase activity and cancer has been shown previously, but there has been little evidence for a causal relationship between the two," said Nakamura. "Having the human telomerase gene may aid in testing the relationship."
The discovery of the gene for the protein called Telomerase Reverse Transcriptase is reported in the Aug. 15 issue of Science.
Authors of the Science paper include Nakamura, Joachim Lingner and Thomas Cech of CU-Boulder and the Howard Hughes Medical Institute, and Gregg Morin, Karen Chapman, Scott Weinrich, William Andrews and Calvin Harley of Geron Corp. of Menlo Park, Calif.
Before the discovery of the telomerase gene, "Cancer researchers
knew telomerase only indirectly, by following the reaction it catalyzed,"
said Cech, who shared the 1989 Nobel prize for chemist
Contact: Thomas Cech
University of Colorado at Boulder