Biology of restriction-modification systems at the single-cell and population level (Record no. 373545)

000 -LEADER
fixed length control field 02753nam a22003377a 4500
003 - CONTROL NUMBER IDENTIFIER
control field AT-ISTA
005 - DATE AND TIME OF LATEST TRANSACTION
control field 20190813094448.0
008 - FIXED-LENGTH DATA ELEMENTS--GENERAL INFORMATION
fixed length control field 180627b xxu||||| |||| 00| 0 eng d
040 ## - CATALOGING SOURCE
Transcribing agency IST
100 ## - MAIN ENTRY--PERSONAL NAME
Personal name Pleska, Maros
9 (RLIN) 4279
245 ## - TITLE STATEMENT
Title Biology of restriction-modification systems at the single-cell and population level
260 ## - PUBLICATION, DISTRIBUTION, ETC. (IMPRINT)
Name of publisher, distributor, etc. IST Austria
Date of publication, distribution, etc. 2017
500 ## - GENERAL NOTE
General note Thesis
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Formatted contents note Abstract
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Formatted contents note Acknowledgments
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Formatted contents note Preface
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Formatted contents note About the author
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Formatted contents note List of publications appearing in thesis
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Formatted contents note Table of contents
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Formatted contents note List of figures
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Formatted contents note List of tables
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Formatted contents note List of symbols/abbreviations
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Formatted contents note 1 Introduction
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Formatted contents note 2 Effects of mutations in phage restriction sites during escape from restriction-modification
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Formatted contents note 3 Bacterial autoimmunity due to a restriction-modification system
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Formatted contents note 4 Phage-host population dynamics promotes prophage acquisition in bacteria with innate immunity
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Formatted contents note References
520 ## - SUMMARY, ETC.
Summary, etc. Restriction-modification (RM) represents the simplest and possibly the most widespread mechanism of self/non-self discrimination in nature. In order to provide bacteria with immunity against bacteriophages and other parasitic genetic elements, RM systems rely on a balance between two enzymes: the restriction enzyme, which cleaves non-self DNA at specific restriction sites, and the modification enzyme, which tags the host’s DNA as self and thus protects it from cleavage. In this thesis, I use population and single-cell level experiments in combination with mathematical modeling to study different aspects of the interplay between RM systems, bacteria and bacteriophages. First, I analyze how mutations in phage restriction sites affect the probability of phage escape – an inherently stochastic process, during which phages accidently get modified instead of restricted. Next, I use single-cell experiments to show that RM systems can, with a low probability, attack the genome of their bacterial host and that this primitive form of autoimmunity leads to a tradeoff between the evolutionary cost and benefit of RM systems. Finally, I investigate the nature of interactions between bacteria, RM systems and temperate bacteriophages to find that, as a consequence of phage escape and its impact on population dynamics, RM systems can promote acquisition of symbiotic bacteriophages, rather than limit it. The results presented here uncover new fundamental biological properties of RM systems and highlight their importance in the ecology and evolution of bacteria, bacteriophages and their interactions.
856 ## - ELECTRONIC LOCATION AND ACCESS
Uniform Resource Identifier <a href="https://doi.org/10.15479/AT:ISTA:th_916">https://doi.org/10.15479/AT:ISTA:th_916</a>
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  Not Lost       Library Library 2018-06-27 AT-ISTA#001534 2018-11-06 2018-06-27 Book

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