Accepted_test

Systematic analysis of tandem genome amplification events in Yersinia pestis
by Konanov D.N. | Liubimova O.N. | Kovrizhnikov A.V. | Sonets I.V. | Balykova A.N. | Lukina-Gronskaya A.V. | Speranskaya A.S. | Eroshenko G.A. | Ilina E.N. | Govorun V.M. | Kutyrev V.V. | Research Institute for System Biology and Medicine of Rospotrebnadzor | Moscow Institute of Physics and Technology (National Research University) | Russian Research Anti-Plague Institute “Microbe” | Research Institute for System Biology and Medicine of Rospotrebnadzor | Russian Research Anti-Plague Institute “Microbe” | Research Institute for System Biology and Medicine of Rospotrebnadzor | Research Institute for System Biology and Medicine of Rospotrebnadzor | Russian Research Anti-Plague Institute “Microbe” | Research Institute for System Biology and Medicine of Rospotrebnadzor | Research Institute for System Biology and Medicine of Rospotrebnadzor | Russian Research Anti-Plague Institute “Microbe”
Abstract ID: 151
Event: BGRS-abstracts
Sections: [Sym 1] Section “Structural-functional organization of genomes and transcriptomics”

Tandem genome amplification is quite common in bacteria growing under stress conditions while spontaneous genome amplification events are rare, not stable and generally poorly described. In most cases, tandem amplification is a result of RecA-dependent recombination which requires short DNA repeats flanking the amplified region. Plague pathogen Yersinia pestis is a unique organism that contains an enormous number of short repeat sequences in its genome and as a result is prone to spontaneous genome rearrangements including large tandem duplication events. Now, rearrangement dynamics in Y. pestis is considered as one of its main adaptation mechanisms, and we suppose that genome amplification events also might play a role in it by affecting gene expression. In this study, we aimed to systematically consider the frequency of spontaneous genome amplification events in Y. pestis, identify their main drivers and analyze the gene content of the amplified regions.