title: ÐÐ¾Ð´ÐµÐ»Ð¸ÑÐ¾Ð²Ð°Ð½Ð¸Ðµ Ð´Ð¸Ð½Ð°Ð¼Ð¸ÐºÐ¸ ÑÑÐ°Ð½ÑÐ¿Ð¾Ð·Ð¾Ð½Ð¾Ð² Ð² Ð³ÐµÐ½Ð¾Ð¼Ðµ
title: Ð²ÑÐ¿ÑÑÐºÐ½Ð°Ñ ÐºÐ²Ð°Ð»Ð¸ÑÐ¸ÐºÐ°ÑÐ¸Ð¾Ð½Ð½Ð°Ñ ÑÐ°Ð±Ð¾ÑÐ° Ð±Ð°ÐºÐ°Ð»Ð°Ð²ÑÐ°
titleType: Subtitle
title: Modelling of the dynamics of transposons in the genome
Creators: name: Ð¢Ð¸Ð¼Ð¾ÑÐµÐµÐ², ÐÐ»ÐµÐºÑÐ°Ð½Ð´Ñ
Publisher: name: Ð¡Ð°Ð½ÐºÑ-ÐÐµÑÐµÑÐ±ÑÑÐ³ÑÐºÐ¸Ð¹ Ð¿Ð¾Ð»Ð¸ÑÐµÑÐ½Ð¸ÑÐµÑÐºÐ¸Ð¹ ÑÐ½Ð¸Ð²ÐµÑÑÐ¸ÑÐµÑ ÐÐµÑÑÐ° ÐÐµÐ»Ð¸ÐºÐ¾Ð³Ð¾
Year: 2022
Subjects: ÑÑÐ°Ð½ÑÐ¿Ð¾Ð·Ð¾Ð½Ñ
Ð°Ð½Ð°Ð»Ð¸Ð· ÑÑÑÐ¾Ð¹ÑÐ¸Ð²Ð¾ÑÑÐ¸
Ð¼Ð¾Â­Ð´ÐµÐ»Ñ Ñ Ð¸ÑÐ½Ð¸Ðº-Ð¶ÐµÑÑÐ²Ð°
transposons
stability analysis
predator-prey model

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description: The subject of the graduate qualification work is Â«Modelling of the dynamics oftransposons in the genomeÂ».Transposons are mobile genetic elements that can reproduce and relocate withinhost genome. Increased activity in their transposition may be observed in variousdeceases, including cancer. This work aimed to study the interaction between anautonomous (L1) and a non-autonomous (Alu) transposons. Autonomous transposonsencode the enzymes that are required for their replication. Non-autonomous transposonsuse expression products of autonomous transposons for reproduction. In the present worktwo transposon dynamics models were developed and studied. The first one describesthe dynamics within one cell taking pseudogenes into account. Pseudogenes are geneticelements that may appear in the genome as a result of reverse-transription of mRNA.Some of them are also able to replicate using the same mechanism. For the initialinsertion and for the replication pseudogenes may, just like non-autonomous transposons,use expression products of L1. Besides that, pseudogenes also compete with transposonsfor cellular resources (ribosomes). This study showed that the double role of pseudogenesin case of increased competition leads to a dynamics that is substantially different fromwhat may be observed in case of increased competition with the rest of the genes. Thesecond model describes the dynamics of autonomous and non-autonomous transposonsin a population of cells. It takes into account natural selection and the mutagenic influenceof transposons. Within the framework of the population model it was shown that theinteration between the two types of transposons leads to fluctuations in number of theircopies and in the population size. A difference was found in the influence of parametersthat determine the negative impact of autonomous and non-autonomous transposons onthe oscillation period. The resulting models can be used to understand the mechanismsof transposon replication in populations of cells with a high transposition rate (forexample, in cancer cells), taking into account their interaction with other cellular agents.