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Genetic analysis of arabidopsis metacaspases as regulators of responses to DNA damage in root stem cells

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TitleInfo
Title
Genetic analysis of arabidopsis metacaspases as regulators of responses to DNA damage in root stem cells
Name (type = personal)
NamePart (type = family)
Chen
NamePart (type = given)
Chia-Hui
NamePart (type = date)
1986-
DisplayForm
Chia-Hui Chen
Role
RoleTerm (authority = RULIB)
author
Name (type = personal)
NamePart (type = family)
Lam
NamePart (type = given)
Eric
DisplayForm
Eric Lam
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
chair
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)
2016
DateOther (qualifier = exact); (type = degree)
2016-10
CopyrightDate (encoding = w3cdtf); (qualifier = exact)
2016
Place
PlaceTerm (type = code)
xx
Language
LanguageTerm (authority = ISO639-2b); (type = code)
eng
Abstract (type = abstract)
Metacaspases (MCPs), are highly conserved caspase-related cysteine proteases that may play important roles in controlling programmed cell death (PCD) in plants. Arabidopsis thaliana has nine metacaspases, and they could be divided into Type Ⅰ
(AtMC1-3) and Type Ⅱ(AtMC4-9), based on their predicted protein sequences. Recent research indicates the function for some of the AtMCs; however, there are many difficulties in studying plant PCD: Single gene mutations produce only quantitative effects and are often quite variable, suggesting that potential functional redundancy among members of this multigene family and parallel pathways may confound interpretation of phenotypes. In this thesis work, I explored a well-defined DNA damage response (DDR) of root stem cells as an excellent cellular model for PCD studies in plants. Root stem cells have been shown to exhibit low resistance to genotoxic stresses. To maintain the integrity of the genome, plant root stem cells induce different downstream consequences such as DNA repair mechanisms, cell-cycle arrest, or PCD upon excess DNA damage that is correlated with elongation arrest of the root. Compared with wild-type plants, the root tip of atmc2, atmc4, atmc2/4, atmc9 and atmc4/9 gene knockout mutants show a lower suppression effect of primary root elongation after zeocin treatment, a genotoxic radiomimetic drug that initially causes cell death in the root stem cell niche and inducing DNA double-strand breaks (DSBs). Among these 3 AtMC genes studied, my results showed that atmc9 mutant displayed the highest resistance to zeocin treatment and but no significant difference between the atmc4/9 double mutant and the single gene mutants in terms of root elongation. Interestingly, the atmc4/9 double mutant showed a dramatic suppression of PCD at the root stem cell niche compared to the other genotypes examined. Taken together, these results indicate that AtMC2, AtMC4, and AtMC9 might work as positive regulators in the Zeocin-activated PCD process in the Arabidopsis root stem cell niche and AtMC9 plays the most important role than other two genes.
Subject (authority = RUETD)
Topic
Plant Biology
RelatedItem (type = host)
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Rutgers University Electronic Theses and Dissertations
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ETD
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ETD_7692
PhysicalDescription
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electronic resource
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application/pdf
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text/xml
Extent
1 online resource (ix, 48 p. : ill.)
Note (type = degree)
M.S.
Note (type = bibliography)
Includes bibliographical references
Note (type = statement of responsibility)
by Chia-Hui Chen
RelatedItem (type = host)
TitleInfo
Title
Graduate School - New Brunswick Electronic Theses and Dissertations
Identifier (type = local)
rucore19991600001
Location
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NjNbRU
Identifier (type = doi)
doi:10.7282/T3QF8W54
Genre (authority = ExL-Esploro)
ETD graduate
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Rights

RightsDeclaration (ID = rulibRdec0006)
The author owns the copyright to this work.
RightsHolder (type = personal)
Name
FamilyName
Chen
GivenName
Chia-Hui
Role
Copyright Holder
RightsEvent
Type
Permission or license
DateTime (encoding = w3cdtf); (qualifier = exact); (point = start)
2016-09-29 22:53:21
AssociatedEntity
Name
Chia-Hui Chen
Role
Copyright holder
Affiliation
Rutgers University. Graduate School - New Brunswick
AssociatedObject
Type
License
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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)
2016-10-31
DateTime (encoding = w3cdtf); (qualifier = exact); (point = end)
2017-10-31
Type
Embargo
Detail
Access to this PDF has been restricted at the author's request. It will be publicly available after October 31st, 2017.
Copyright
Status
Copyright protected
Availability
Status
Open
Reason
Permission or license
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ETD
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windows xp
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DateCreated (point = end); (encoding = w3cdtf); (qualifier = exact)
2016-09-30T02:37:52
DateCreated (point = end); (encoding = w3cdtf); (qualifier = exact)
2016-09-30T02:37:52
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