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Technion researchers have discovered how an essential enzyme binds to the ends of chromosomes

Understanding the process is important for controlling the enzyme and inhibiting it, for the purpose of curing diseases

Researchers at the Faculty of Biology at the Technion were able to discover how the enzyme telomerase binds to the ends of chromosomes. Understanding the process is essential for controlling the enzyme and inhibiting it in order to cure diseases. The discovery was published in the latest issue of PNAS, the scientific journal of the American National Academy of Sciences.
"The ends of the chromosomes, called telomeres and containing DNA and proteins, are of particular importance," explains Professor Haim Menor, who heads the team that carried out the research. "Their importance stems from the fact that they protect the chromosomes from damage that causes cell death, or cancer."
The synthesis of telomeres requires a special enzyme called telomerase, which lengthens the telomeric DNA. Cancer cells contain a high concentration of telomerase, unlike normal cells. Therefore, substances that inhibit the activity of telomerase are expected to be selective drugs for curing cancer, which will hardly cause side effects.
It is also expected that the introduction of transgenic telomerase into stem cells will cause the cells to multiply. In this way, the enzyme will be used for tissue engineering, that is, for the growth of tissues and organs that will contain a large number of cells and will be used for transplantation.
A more distant possibility stems from the discovery that the telomeres in the cells of old people are shorter than the telomeres in the cells of young people. This discovery led to the hypothesis that telomere shortening is an important factor in the aging process. Therefore, the possibility is raised that cells containing transgenic telomerase will be inserted into the body of humans and cause the aging process to be delayed and their lives to be extended. 
In order to engineer telomerase, optimize it and know how to inhibit it, it was important to discover how it interacts with telomeres. Indeed, the Technion researchers found the location where the attachment takes place, that is, the location in the enzyme to which the telomeric DNA binds. Part of this research was included in the master's thesis of Erez Rumi, who was a student in the laboratory of Professor Haim Menor and even carried out an important part of the continuation of the research, which was conducted in collaboration with the laboratory of Professor Kathleen Collins at the University of California at Berkeley. The research was carried out on telomerase originating from the cilia, where the enzyme was first discovered in 1985 by Professor Elizabeth Blackburn and Carol Greider in their laboratory in the USA. The use of telomerase from Marisin for the research conducted at the Technion was due to the fact that until now this enzyme was the only one with which the experiments that led to the above results could be performed. It is worth noting, however, that the telomerase from marigold is similar to the telomerase found in human cells and therefore it is expected that the binding to DNA is carried out in a similar way in the human enzyme.  

 

One response

  1. The mere fact that telomeres in adults are shorter than those in young people is not proof that the suppression of telomerase activity is directly involved in aging. Mice have much longer telomeres than ours and their life spans are significantly shorter.
    Aging is a complex multi-causal process (oxygen free radicals as the main factor) and the shortening of telomeres is just a result of cell division. In our bodies, there is a controlled activity of telomerase in stem cells, this is to allow them to continue dividing many times without the chromosomes being damaged. In my opinion, telomerase is essential for maintaining the integrity of DNA in many divisions and the suppression of its activity in sorted cells stems firstly from a lack of necessity (=saving energy) and secondly as a preventive mechanism for cancerous transformation.

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