Categorized | Anti Aging

Molecular Switch Used By Telomerase for Extension of Telomere Identified

For the first time, investigators from the University Of Illinois College Of Medicine at Chicago illustrated that steady preservation of chromosome ends by telomerase can be enabled by chemical modification of a prime suspect of DNA damage checkpoint enzymes. Researchers believe that telomerase play a vital role in aging and cancer.

Study findings are published in Nature Structural and Molecular Biology.

Telomerase is an enzyme complex that plays an important role in the maintenance of telomere. In the absence of telomerase, telomere turns out to be gradually shorter whenever division of cell occurs.

If telomeres continue to get short, then a point will arrive where chromosome ends will be considered as wrecked, enabling DNA-damage checkpoint proteins to stop further division of cells and DNA repair proteins to rearrange or combine the chromosome ends.

This dysfunction of telomere has been associated with premature aging and tumor formation in humans.

Toru Nakamura, leader of the UIC study, drove his focus on determining how ATR and ATM –2 DNA-damage checkpoint enzymes, contribute to telomerase regulation.

“Our research showed that ATR and ATM enable switching one of the telomere complexes by chemical modification of a definite target protein attached to the DNA of telomere, which then draws telomerase,” Nakamura said.

Fission yeast cells were used in the study as they utilize protein complexes identical to those utilized by human cells for telomere maintenance.

According to Nakamura, an identical ATR/ATM-dependent molecular switch may be there in human cells too for regulating the maintenance of telomere. However, some differences may be there at protective complex regulation, he noted.

As any dysfunction in regulation of telomere maintenance procedures is responsible for tumor formation, cancers can be prevented by having proper knowledge of collaboration of cellular components for the generation of functional telomeres, Nakamura said.