The 2009 Nobel Prize in Biology and Medicine for “the discovery of telomerase and the role of this enzyme in protecting the ends of chromosomes” was awarded to three prominent scientists from the United States.
The wave of official outrage is supported in scientific forums by representatives of the general scientific community. It is argued that the function of telomeres was accurately predicted by Alexey Olovnikov, and the work of the laureates only confirmed this hypothesis with more than a ten-year delay. The hysteria about the fact that an Englishwoman (American, Swedish – underline as necessary) is intriguing and therefore does not allow us in general, and our science in particular, to take a proper (i.e. leading) place in the world table of ranks, could be a subject for psychiatric and collective unconscious specialists and say a lot about our complexes. As for the RAS “grievances,” Olovnikov’s outstanding work was not enough in the eyes of the Biology Department of the RAS to get him elected even as a corresponding member. In this situation, to complain about the lack of recognition abroad is at least illogical (by the way, all three laureates are members of the National Academy of Sciences of the United States).

What is the essence of the Nobel results of Blackburn, Shostak and Greider, and how do they correlate with Olovnikov’s hypothesis? Telomeres are the ends of linear chromosomes. The role of telomeres in ensuring the “correctness” and stability of chromosome inheritance became apparent as early as the 1930s (by correctness and stability we mean that each of the daughter cells receives the entire set of maternal chromosomes and this process can occur an infinite number of times). It was also understood that telomeres of different chromosomes were interchangeable. At the beginning of the 1980s, the mechanism of the stabilizing function of chromosomes was unknown. The main focus of Liz Blackburn’s scientific work before her Nobel results was to study the linear DNA of the infusoria Tetrahymena. This single-celled organism has a gigantic size compared to normal cells, and therefore the genes in the genome itself are not sufficient to meet the needs of the huge volume of cytoplasm. The problem is solved by amplification (increasing the number of copies) of some important genes. In this case, each amplified gene is located on a separate linear DNA molecule. These linear molecules are “properly” distributed into daughter cells, i.e. they behave as mini-chromosomes. The ends of such mini-chromosomes can be considered as telomeres.

The study of the mechanisms of inheritance of mini-chromosomes in infusoria (a fundamental problem extremely far removed from the needs of the economy, medicine, etc.) was complicated by methodological difficulties of working with infusoria, in particular by the impossibility of using powerful genetic approaches. Jack Szostak studied plasmids – small self-replicating DNA molecules – in yeast, one of the favorite objects of molecular biology and genetics. He showed that while ring plasmids are stably inherited during yeast cell division, linear plasmids, in contrast, are rapidly lost. Although yeast chromosomes are linear, they are not lost and are inherited stably. What is the reason for the different behavior of linear plasmids and chromosomes? In a paper published in 1982, Shostak and Blackburn showed that if the end sites (telomeres) of linear amplified infusoria DNA molecules are placed on the ends of linear yeast plasmids, such hybrid plasmids are stably inherited. After the publication of this work, Shostak did not actually deal with the telomere problem. However, the experimental system he created made it possible to easily detect the function of telomeres (in terms of their ability to ensure stable inheritance of linear plasmids) in yeast. Since molecular biologists have at their disposal a huge arsenal of effective methods for studying yeast, further progress was a matter of technique. Very soon it became clear that the presence of a terminal short DNA sequence was necessary and sufficient to stabilize the inheritance of linear plasmids. This sequence must be repeated several times and is called a telomere repeat. It is very important that it would have been impossible to obtain such data in Tetrahymena, the organism that started it all, neither then nor now.

The fact that the same section of DNA functions both in infusoria and in yeast, organisms that are evolutionarily very far apart, meant that researchers were dealing with a fundamental mechanism that ensures stable inheritance of linear DNA molecules in many or even all living organisms. There could be a great number of such mechanisms (e.g. “looping” of linear DNA molecules at the moment of cell division, when the probability of loss of linear DNA is the highest). The task was to determine which mechanism is actually implemented.