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DNA repair and sister chromatid exchange

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dc.contributor.authorHagelstrom, R. Tanner, author
dc.contributor.authorBailey, Susan M., advisor
dc.contributor.authorLiber, Howard, advisor
dc.date.accessioned2024-03-13T19:53:49Z
dc.date.available2024-03-13T19:53:49Z
dc.date.issued2008
dc.description.abstractMitotic recombination that occurs between sister chromatids, known as sister chromatid exchange (SCE), is a common event in mammalian cells; yet very little is understood about SCE. Likewise, the biological relevance of SCE to humans is also unclear. It is generally thought that SCE represents no permanent alteration to genetic information, however, many cancer prone syndromes present elevated levels of SCE and it is not known whether they are a causal factor in cancer progression or simply a symptom of underlying genomic instability. It has also been purposed that SCE occurring in telomeres (T-SCE) may contribute to the aging phenotype seen in progeroid syndromes. Several accelerated aging syndromes, such as progeria, show highly elevated levels of SCE within telomeric regions. The role of DNA repair in SCE regulation and formation is also under investigation. While it has been shown that at least one of the DNA repair pathways, homologous recombination (HR), is likely to be involved in the formation of SCE, it is less clear whether other DNA repair pathways are also involved in either the formation or suppression of SCE. Therefore, the goal of this research has been to better understand how DNA repair pathways can influence SCE frequency, and how SCE relates to cancer progression and aging. This research also examines how the physical location of SCE, whether it be in genomic (G-SCE) or telomeric (T-SCE) DNA, influence which DNA repair pathways are involved. I examined the role of HR by investigating the Werner (WRN), Bloom (BLM), and FANCD2 proteins. I also investigated the role of non-homologous end joining (NHEJ) by examining the DNA-dependent protein kinase (DNA-PKcs), both the Ku70/80 heterodimer and the catalytic subunit (DNA-PKcs), and Artemis. ERCC1 is a representative member of the final DNA repair pathway examined, nucleotide excision repair (NER). Lastly, I determined if/how DNA repair status can influence the ionizing radiation induced bystander effect (BSE). I was able to determine that at least some of the DNA repair proteins are critical in the generation of a bystander signal providing the first evidence that DNA repair can have an influence via an inter-cellular pathway.
dc.format.mediumborn digital
dc.format.mediumdoctoral dissertations
dc.identifierETDF_Hagelstrom_2008_3321281.pdf
dc.identifier.urihttps://hdl.handle.net/10217/237768
dc.languageEnglish
dc.language.isoeng
dc.publisherColorado State University. Libraries
dc.relation.ispartof2000-2019
dc.rightsCopyright and other restrictions may apply. User is responsible for compliance with all applicable laws. For information about copyright law, please see https://libguides.colostate.edu/copyright.
dc.rights.licensePer the terms of a contractual agreement, all use of this item is limited to the non-commercial use of Colorado State University and its authorized users.
dc.subjectaging
dc.subjectcancer
dc.subjectDNA repair
dc.subjectsister chromatid exchange
dc.subjectmolecular biology
dc.subjectcellular biology
dc.subjectmedicine
dc.subjectoncology
dc.titleDNA repair and sister chromatid exchange
dc.typeText
dcterms.rights.dplaThis Item is protected by copyright and/or related rights (https://rightsstatements.org/vocab/InC/1.0/). You are free to use this Item in any way that is permitted by the copyright and related rights legislation that applies to your use. For other uses you need to obtain permission from the rights-holder(s).
thesis.degree.disciplineCell and Molecular Biology
thesis.degree.grantorColorado State University
thesis.degree.levelDoctoral
thesis.degree.nameDoctor of Philosophy (Ph.D.)

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