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Homologous recombination sites during drosophila female meiosis and the role of the drosophila ino80 complex in meiotic recombination

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TitleInfo
Title
Homologous recombination sites during drosophila female meiosis and the role of the drosophila ino80 complex in meiotic recombination
Name (type = personal)
NamePart (type = family)
Cardona
NamePart (type = given)
Cristina Ochoa
NamePart (type = date)
1979-
DisplayForm
Cristina Ochoa Cardona
Role
RoleTerm (authority = RULIB)
author
Name (type = personal)
NamePart (type = family)
McKim
NamePart (type = given)
Kim S
DisplayForm
Kim S McKim
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
chair
Name (type = personal)
NamePart (type = family)
Kramer
NamePart (type = given)
Sunita-Gupta
DisplayForm
Sunita-Gupta Kramer
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
internal member
Name (type = personal)
NamePart (type = family)
Walworth
NamePart (type = given)
Nancy C
DisplayForm
Nancy C Walworth
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
internal member
Name (type = personal)
NamePart (type = family)
Gartenberg
NamePart (type = given)
Marc
DisplayForm
Marc Gartenberg
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
outside member
Name (type = corporate)
NamePart
Rutgers University
Role
RoleTerm (authority = RULIB)
degree grantor
Name (type = corporate)
NamePart
Graduate School - New Brunswick
Role
RoleTerm (authority = RULIB)
school
TypeOfResource
Text
Genre (authority = marcgt)
theses
OriginInfo
DateCreated (qualifier = exact)
2014
DateOther (qualifier = exact); (type = degree)
2014-10
CopyrightDate (encoding = w3cdtf)
2014
Place
PlaceTerm (type = code)
xx
Language
LanguageTerm (authority = ISO639-2b); (type = code)
eng
Abstract (type = abstract)
DNA Double Strand breaks (DSBs) are one of the most lethal types of genomic damage. Irregularities in the repairs of DSBs can lead to chromosomal aberrations, such as deletions, translocations, and inversions that ultimately are responsible for cancer, infertility, and birth defects. Cells have several conserved and controlled DNA repair pathways, in which a plethora of factors must be activated and recruited to the break. Moreover, eukaryotes must also locally and transiently modify chromatin to allow access of repair factors. Very little is known about chromatin remodeling during DSB processing in higher eukaryotes, partially due to the lack of suitable study models. Here I used Drosophila female meiosis as the model and show the development of a marker and fixation protocol that enables the labeling and following of DSB sites during recombinational repair. Moreover, I provide evidence that early and late repair sites correspond to non-crossovers (NCO) and crossovers (CO), respectively. In the next part of this study, I provide novel evidence that: 1) COs persist longer than NCOs and are mobilized to the nuclear periphery, 2) movement of COs to the periphery is developmentally controlled, depends on ATR, and occurs during mid-pachytene when NCOs are repaired, 3) any persisting DSB can form MRN foci that are mobilized to the periphery from mid-pachytene on. Furthermore, I focus on the role of dINO80, an ATP-dependent chromatin remodeler, during meiotic recombination. To date it has never been shown that INO80 has a role in meiosis or whether it functions in early recognition steps. Here I show that Ino80, the catalytic subunit of the INO80 complex, interacts in a damage dependent fashion with components of the MRN complex, and that Ino80 is required for the recognition of the majority of meiotic DSBs. Furthermore this study suggests that the ATP-dependent remodeling function of dIno80 is crucial for its role in recognition of meiotic DSBs. Drosophila female meiosis in conjunction with the developed techniques in this study provide a powerful system to study the dynamics of meiotic DSB sites and to spatially and temporally dissect the role of chromatin modifying complexes in DSB repair.
Subject (authority = RUETD)
Topic
Cell and Developmental Biology
Subject (authority = ETD-LCSH)
Topic
DNA repair
Subject (authority = ETD-LCSH)
Topic
DNA recombination
RelatedItem (type = host)
TitleInfo
Title
Rutgers University Electronic Theses and Dissertations
Identifier (type = RULIB)
ETD
Identifier
ETD_5723
PhysicalDescription
Form (authority = gmd)
electronic resource
InternetMediaType
application/pdf
InternetMediaType
text/xml
Extent
1 online resource (ix, 248 p. : ill.)
Note (type = degree)
Ph.D.
Note (type = bibliography)
Includes bibliographical references
Note (type = statement of responsibility)
by Cristina Ochoa Cardona
RelatedItem (type = host)
TitleInfo
Title
Graduate School - New Brunswick Electronic Theses and Dissertations
Identifier (type = local)
rucore19991600001
Location
PhysicalLocation (authority = marcorg); (displayLabel = Rutgers, The State University of New Jersey)
NjNbRU
Identifier (type = doi)
doi:10.7282/T35X27CJ
Genre (authority = ExL-Esploro)
ETD doctoral
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Rights

RightsDeclaration (ID = rulibRdec0006)
The author owns the copyright to this work.
RightsHolder (type = personal)
Name
FamilyName
Cardona
GivenName
Cristina
MiddleName
Ochoa
Role
Copyright Holder
RightsEvent
Type
Permission or license
DateTime (encoding = w3cdtf); (qualifier = exact); (point = start)
2014-06-30 08:23:32
AssociatedEntity
Name
cristina cardona
Role
Copyright holder
Affiliation
Rutgers University. Graduate School - New Brunswick
AssociatedObject
Type
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 (encoding = w3cdtf); (qualifier = exact); (point = start)
2014-10-31
DateTime (encoding = w3cdtf); (qualifier = exact); (point = end)
2016-10-30
Type
Embargo
Detail
Access to this PDF has been restricted at the author's request. It will be publicly available after October 30th, 2016.
Copyright
Status
Copyright protected
Availability
Status
Open
Reason
Permission or license
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Technical

RULTechMD (ID = TECHNICAL1)
ContentModel
ETD
OperatingSystem (VERSION = 5.1)
windows xp
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