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Telomeres are the protective caps at the ends of chromosomes. In adult cells, telomeres shorten each time a cell divides and this contributes to aging and cancer. Pluripotent stem cells, however, are specialized cells that exist in the early days of development. These pluripotent cells do not age and have the ability to transform into any type of adult cell.
The surprise discovery, published today in Nature, shows that telomeres in pluripotent stem cells are protected very differently from telomeres in adult tissues.
“This disrupts 20 years of thinking about how stem cells protect their DNA,” said Associate Professor Tony Cesare, of the University of Sydney’s School of Medicine and Health, who heads the Genome Integrity Unit at Children’s Medical. Research Institute (CMRI) and co-leader of a research group that collaborated on this research.
In adult cells, a protein called TRF2 is essential because it arranges the DNA at the end of the chromosome in a “telomere loop” structure. Removing TRF2 from adult cells causes the chromosomes to be stitched together in a long string, which is incompatible with life.
To the researchers’ amazement, removing TRF2 from pluripotent stem cells did next to nothing. The chromosomes were normal, the telomeres remained and the cells divided as if nothing had happened. Telomeres are therefore protected differently in pluripotent stem cells and in adult tissues.
This unexpected discovery has important implications for research on aging, human development, regenerative medicine and cancer. Previously, researchers expected that the fundamental mechanisms that protected DNA would be the same in all tissues. This now appears to be incorrect.
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