The number of times our cells can divide is dictated by telomeres, stretches of DNA at the tips of our chromosomes. Understanding how telomeres keep our chromosomes—and by extension, our genetic
makeup—intact is an area of intense scientific focus in the fields of both aging and cancer. Now, the laboratory of Emmanuel Skordalakes, Ph.D., assistant professor in Wistar’s Gene Expression and Regulation Program, has published the first detailed report that highlights the structure and function of Cdc13, a protein that sustains telomeres by clamping to DNA and recruiting important enzymes to the area.
While the nature of Cdc13 had previously eluded scientists, the Wistar researchers found that two copies of the protein bind together to form what is called a “dimer” [pronounced DYE-mer]. They also showed that the dimer physically interacts with DNA, regulating how the enzyme telomerase lengthens the telomeres. Skordalakes published his findings in the journal Molecular and Cellular Biology.
“Cdc13 has a crucial support role in maintaining and lengthening telomeres, which are
reduced in length through every round of DNA replication,” said Skordalakes. “We know that disabling this protein in humans will most likely lead to cell death, which is of particular interest in cancer, because telomere lengthening is one of the ways cancer cells obtain their immortality.”