Dr. Woodring E. Wright, Professor of Cell Biology and Internal Medicine, and Dr. Jerry W. Shay, Professor and Vice Chairman of Cell Biology at UT Southwestern. Credit: UT Southwestern Medical Center
An article in MedicalXpress.com explains:
A novel looping mechanism that involves the end caps of DNA may help explain the aging of cells and how they initiate and transmit disease, according to new research from UT Southwestern Medical Center cell biologists.Read more here.
The UT Southwestern team found that the length of the endcaps of DNA, called telomeres, form loops that determine whether certain genes are turned off when young and become activated later in life, thereby contributing to aging and disease.
"Our results suggest a potential novel mechanism for how the length of telomeres may silence genes early in life and then contribute to their activation later in life when telomeres are progressively shortened. This is a new way of gene regulation that is controlled by telomere length," said Dr. Jerry W. Shay, Professor and Vice Chairman of Cell Biology at UT Southwestern, who led the team with his colleague, Dr. Woodring E. Wright, Professor of Cell Biology and Internal Medicine.
Telomeres cap the ends of the cell's chromosomes to protect them from damage. But the telomeres become shorter every time the cell divides. Once they shorten to a critical length, the cell can no longer divide and enters into a senescent or growth-arrest phase in which the cell produces different products compared to a young quiescent cell. Most research in this area has focused on the role that the process plays in cancer, but telomere shortening also has been shown to influence which genes are active or silent.
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