Purpose: General information about telomeres, the principles of replication and the problem of
duplication of DNA linear molecule ends caused by the DNA-polymerases inability for primerless
synthesis are considered. The mechanism of eukaryote chromosome DNA end elongation by
telomerase is described. The role of cell telomerase activity in the determination of their
proliferative potential is discussed. The consequences of alterations in the telomere lenghth and the
telomerase activity for cell aging and tumor growth are discussed in this presentation.
Introduction: Telomeres are DNA-protein structures that cap the end of eukaryotic chromosomes.
Telomeric DNA typically consists of numerous tandemly repeated sequences which are synthesized
by unusual RNA-containing enzyme, telomerase.
The continuity of the genetic material in the generations of cells and organisms is ensured by the
process of replication - the doubling of DNA molecules. As a result of this complicated process,
carried out by a complex of several enzymes and proteins lacking the catalytic activity, necessary to
give the polynucleotide chains the necessary conformation, two identical double helices of DNA are
formed. These so-called "daughter" molecules are no different from each other and from the
original "maternal" DNA molecule. Replication occurs in the cell before division, therefore each
daughter cell receives exactly the same DNA molecules as the mother cell had.
The "end-replication problem" is that all known DNA polymerases, which are key enzymes of a
complex replicative protein complex, are incapable of completely replicating the ends of linear
DNA molecules. In order for the cells not to lose part of the genetic material in the fission, the 3'-
ends of the DNA of the eukaryotic chromosomes grow before each round of replication with short
repeating sequences. This is done by enzymes called telomerase.
Results: A.M. Olovnikov put forward a hypothesis about the existence of a special biological
mechanism that solves the problem of terminal replication, suggesting that it acts in the cells of
organisms propagating in vegetative ways, as well as in sex and cancer cells, but does not work in
most of our somatic cells. The building-up of the ends of linear molecules with telomerase is this
mechanism.
Conclusion: If we learn how to control the replication of DNA with the help of telomerase, this
opens wide prospects both in preventing aging and in struggling the cancer.
EXCEL ЭЛЕКТРОН ЖАДВАЛИНИ ҚЎЛЛАШ
Еркебаева А.А. – 2-курс талабаси
Тошкент фармацевтика институти, Тошкент ш.
«Физика, математика ва ахборот технологиялар» кафедраси
Рахбар: к/ӯқитувчи Ш.Т.Ильясов
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