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Role of G9a methyltransferase in the dna damage response signal
Descriptive
TitleInfo
Title
Role of G9a methyltransferase in the dna damage response signal
Name
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Rodriguez-Colon
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Lizahira
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1987-
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Lizahira Rodriguez-Colon
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author
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Xia
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Bing
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Bing Xia
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Advisory Committee
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chair
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Sharon
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Sharon Pine
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Advisory Committee
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internal member
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Ganesan
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Shridar
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Shridar Ganesan
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Advisory Committee
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internal member
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Langer
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Jerome
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Jerome Langer
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Advisory Committee
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Rutgers University
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degree grantor
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School of Graduate Studies
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theses
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2018
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2018-05
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2018
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xx
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eng
Abstract
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DNA damage induces a choreographed set of local changes in histone modifications which leads to efficient recruitment of DNA repair factors. The regulation of these chromatin modifications at DNA breaks is critical to maintain genome integrity. Recent studies in our lab have identified a role for G9a methyltransferase in regulating DNA repair. The overall aim of this project was to elucidate how G9a activity regulates this pathway and to identify the effects of its inhibition in this process. It was shown that G9a localizes to sites of DNA damage in an ATM-dependent fashion and that inhibition of G9a activity affects early recruitment of multiple DNA repair factors. We found that catalytic inhibition of G9a using UNC0638 results in increased ATM activation. This led to increased "spreading" of pH2AX and MDC1 signals seen at regions of localized DNA breaks induced by UV-laser scissors, which was dependent upon ATM activation. This was also associated with increased levels of H3K36me2 and H3K56Ac. Biochemical data showed that G9a interacts and regulates HDAC1/2 activity during the DNA damage response. G9a inhibition led to decreased HDAC1 methylation, and increased ATM acetylation. These data suggest that G9a activity regulates the extent of ATM activation induced by DNA breaks and is required for efficient recruitment of downstream DNA repair factors. Overall our data suggests that G9a plays a critical role in regulation of ATM-dependent signaling during the DNA damage response and raises the possibility of using G9a inhibitors in the clinical setting as part of novel cancer therapies.
Subject
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Topic
Pharmacology, Cellular and Molecular
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Rutgers University Electronic Theses and Dissertations
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ETD_8870
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electronic resource
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Extent
1 online resource (viii, 115 p. : ill.)
Note
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Ph.D.
Note
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Includes bibliographical references
Subject
(authority = ETD-LCSH)
Topic
DNA repair
Note
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by Lizahira Rodriguez-Colon
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School of Graduate Studies Electronic Theses and Dissertations
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rucore10001600001
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Identifier
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doi:10.7282/T3JS9TW0
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ETD doctoral
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Rights
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The author owns the copyright to this work.
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Name
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Rodriguez-Colon
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Lizahira
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Permission or license
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2018-04-12 22:35:00
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Lizahira Rodriguez-Colon
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Rutgers University. School of Graduate Studies
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Author Agreement License
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I hereby grant to the Rutgers University Libraries and to my school the non-exclusive right to archive, reproduce and distribute my thesis or dissertation, in whole or in part, and/or my abstract, in whole or in part, in and from an electronic format, subject to the release date subsequently stipulated in this submittal form and approved by my school. I represent and stipulate that the thesis or dissertation and its abstract are my original work, that they do not infringe or violate any rights of others, and that I make these grants as the sole owner of the rights to my thesis or dissertation and its abstract. I represent that I have obtained written permissions, when necessary, from the owner(s) of each third party copyrighted matter to be included in my thesis or dissertation and will supply copies of such upon request by my school. I acknowledge that RU ETD and my school will not distribute my thesis or dissertation or its abstract if, in their reasonable judgment, they believe all such rights have not been secured. I acknowledge that I retain ownership rights to the copyright of my work. I also retain the right to use all or part of this thesis or dissertation in future works, such as articles or books.
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2018-05-31
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2020-05-30
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Detail
Access to this PDF has been restricted at the author's request. It will be publicly available after May 30th, 2020.
Copyright
Status
Copyright protected
Availability
Status
Open
Reason
Permission or license
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2018-04-18T21:33:19
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