Human telomerase threatens genome integrity by adding telomeres to broken chromosomes and is held in check by ATR kinase signaling.

One of the ways cells in different kinds of tissue communicate is by exchanging RNA molecules. In experiments with roundworms of the species Caenorhabditis elegans, researchers at the State University of Campinas (UNICAMP) in Brazil found that when this communication pathway is dysregulated, the organism’s lifespan is shortened.

An article on the study is published in the journal Gene. The findings contribute to a better understanding of the aging process and associated diseases.

“Previous research showed that some types of RNA can be transferred from one cell to another, mediating intertissue communication, of the kind that occurs with proteins and metabolites, for example. This is considered a mechanism for signaling between organs or neighboring cells. It’s part [of the physiopathology] of several diseases and of the organism’s normal functioning,” said Marcelo Mori, corresponding author of the article and a professor at the Institute of Biology (IB-UNICAMP).

The natural ends of chromosomes appear alarmingly like broken DNA, much as a snapped spaghetti strand is difficult to distinguish from its intact counterparts. Yet every cell in our bodies must have a way of differentiating between the two because the best way to protect the healthy end of a chromosome also happens to be the worst way to repair damaged DNA.

Consider the enzyme telomerase, which is responsible for maintaining protective telomeres at the natural ends of chromosomes. Were telomerase to seal off a broken strand of DNA with a telomere, it would prevent further repair of that break and delete essential genes.

Now, a new study in Science describes how cells avoid such mishaps. These findings show that telomerase can indeed run amok, adding telomeres to damaged DNA, and would do so were it not for the ATR kinase, a key enzyme that responds to DNA damage.