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Homologous recombination: a Swiss Army knife for protecting genome integrity

Claussin, C. 2017 [Groningen]: University of Groningen. 130 p.

Research output: ScientificDoctoral Thesis

Documents

  • Title and contents

    Final publisher's version, 365 KB, PDF-document

  • Chapter 1

    Final publisher's version, 855 KB, PDF-document

  • Chapter 2

    Final publisher's version, 1 MB, PDF-document

  • Chapter 3

    Final publisher's version, 2 MB, PDF-document

  • Chapter 4

    Final publisher's version, 2 MB, PDF-document

    Embargo ends: 22/03/2018

  • Chapter 5

    Final publisher's version, 1 MB, PDF-document

    Embargo ends: 22/03/2018

  • Chapter 6

    Final publisher's version, 957 KB, PDF-document

  • Appendices

    Final publisher's version, 1 MB, PDF-document

  • Complete thesis

    Final publisher's version, 7 MB, PDF-document

    Embargo ends: 22/03/2018

  • Propositions

    Final publisher's version, 79 KB, PDF-document

The genetic information required for life is stored in our DNA. However, every day our cells are exposed to variety of DNA damaging agents. Additionally, endogenous metabolic processes can also be a source of DNA damage. An inability to properly repair DNA leads to genome instability, which is a hallmark of both ageing and cancer. To protect genome integrity, cells have developed pathways to repair DNA damage. Homologous recombination (HR), a major DNA repair pathway, is often associated with the repair of DNA double-strand breaks (DSBs). A DSB is the most lethal type of DNA damage; one single unrepaired DSB is enough to kill a cell. During my PhD, I have been particularly interested in understanding how HR is used to maintain genome integrity, both generally throughout the entire genome and specifically at telomeres. Telomeres are nucleoprotein structures located at the ends of linear chromosomes that help cells distinguish chromosome ends from DSBs. Telomeres shorten due to incomplete DNA replication and nucleolytic degradation. Telomere shortening is also associated with ageing. I have shown that HR proteins are important to repair damage at telomeres, thereby preventing accelerated cellular ageing. I have also quantified HR activity genome-wide by measuring and mapping HR events known as sister chromatid exchanges (SCEs). SCEs are commonly thought to occur as a result of DSB repair, but I have determined that this is not the case for the majority of spontaneous SCE events that occur in wild-type cells.
Original languageEnglish
QualificationDoctor of Philosophy
Awarding Institution
Supervisors/Advisors
Award date22-Mar-2017
Place of Publication[Groningen]
Publisher
Print ISBNs978-90-367-9549-4
Electronic ISBNs978-90-367-9548-7
StatePublished - 2017

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