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53BP1 regulates dna double-strand break repair in a mouse “BRCA-like” model by a non-resection mechanism
Descriptive
TitleInfo
Title
53BP1 regulates dna double-strand break repair in a mouse “BRCA-like” model by a non-resection mechanism
Name
(type = personal)
NamePart
(type = family)
Misenko
NamePart
(type = given)
Sarah Marie
NamePart
(type = date)
1990-
DisplayForm
Sarah Marie Misenko
Role
RoleTerm
(authority = RULIB)
author
Name
(type = personal)
NamePart
(type = family)
Bunting
NamePart
(type = given)
Samuel F
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Samuel F Bunting
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Advisory Committee
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chair
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Steward
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Ruth
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Ruth Steward
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Advisory Committee
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(authority = RULIB)
internal member
Name
(type = personal)
NamePart
(type = family)
Jin
NamePart
(type = given)
Victor
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Victor Jin
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Advisory Committee
Role
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(authority = RULIB)
internal member
Name
(type = personal)
NamePart
(type = family)
Denzin
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(type = given)
Lisa
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Lisa Denzin
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Advisory Committee
Role
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(authority = RULIB)
outside member
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NamePart
Rutgers University
Role
RoleTerm
(authority = RULIB)
degree grantor
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School of Graduate Studies
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school
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Text
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theses
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2017
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2017-10
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2017
Place
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xx
Language
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eng
Abstract
(type = abstract)
DNA end resection is believed to be a step that influences the choice between the two major DNA double-strand break (DSB) repair pathways: homologous recombination (HR) and non-homologous end joining (NHEJ). Deficiencies in either of these pathways can increase predisposition to cancer, a common example being BRCA1 deficient breast and ovarian cancer. Specifically, cells deficient in HR have been considered to be “BRCA-like”. BLM/Dna2 and Exo1 serve as the two main pathways for long-range resection in yeast, but the significance of long-range resection for genome maintenance has not been shown in a primary mammalian model. We found that BlmΔ/ΔExo1-/- cells show synergistic genomic instability compared to single knockout controls, reduced resection, and decreased HR. BlmΔ/ΔExo1-/- cells also show a defect in the G2M checkpoint, attributed to a lack of resected DNA to maintain the checkpoint activation. This suggests that co-deletion of BLM and Exo1 abolishes long-range resection resulting in a “BRCA-like” model. Deleting 53BP1, a protein believed to block resection, restores genomic integrity and HR in BlmΔ/ΔExo1-/- cells, but resection is not restored. This data suggests a role for 53BP1 in restoring HR that is independent of its role in inhibiting DNA end resection.
Subject
(authority = RUETD)
Topic
Biochemistry
Subject
(authority = ETD-LCSH)
Topic
DNA damage
Subject
(authority = ETD-LCSH)
Topic
DNA repair
RelatedItem
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Title
Rutgers University Electronic Theses and Dissertations
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ETD_8299
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electronic resource
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application/pdf
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text/xml
Extent
1 online resource (x, 118 p. : ill.)
Note
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Ph.D.
Note
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Includes bibliographical references
Note
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by Sarah Marie Misenko
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TitleInfo
Title
School of Graduate Studies Electronic Theses and Dissertations
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rucore10001600001
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NjNbRU
Identifier
(type = doi)
doi:10.7282/T3GF0XNM
Genre
(authority = ExL-Esploro)
ETD doctoral
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Rights
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The author owns the copyright to this work.
RightsHolder
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Name
FamilyName
Misenko
GivenName
Sarah
MiddleName
Marie
Role
Copyright Holder
RightsEvent
Type
Permission or license
DateTime
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(point = start)
2017-08-22 11:28:06
AssociatedEntity
Name
Sarah Misenko
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Affiliation
Rutgers University. School of Graduate Studies
AssociatedObject
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License
Name
Author Agreement License
Detail
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.
RightsEvent
DateTime
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2017-10-31
DateTime
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2018-05-02
Type
Embargo
Detail
Access to this PDF has been restricted at the author's request. It will be publicly available after May 2nd, 2018.
Copyright
Status
Copyright protected
Availability
Status
Open
Reason
Permission or license
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Technical
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ETD
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windows xp
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2017-08-24T21:55:17
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