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Roles of carboxypeptidase E (CPE) in regulation of the microtubule cytoskeleton, neuronal migration, and dendrite morphology
Descriptive
TitleInfo
Title
Roles of carboxypeptidase E (CPE) in regulation of the microtubule cytoskeleton, neuronal migration, and dendrite morphology
Name
(type = personal)
NamePart
(type = family)
Liang
NamePart
(type = given)
Chen
NamePart
(type = date)
1988-
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Chen Liang
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(authority = RULIB)
author
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(type = personal)
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Firestein
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(type = given)
Bonnie L
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Bonnie L Firestein
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Advisory Committee
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chair
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D'Arcangelo
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Gabriella
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Gabriella D'Arcangelo
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Advisory Committee
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internal member
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(type = personal)
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(type = family)
Rasin
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Mladen-Roko
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Mladen-Roko Rasin
Affiliation
Advisory Committee
Role
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(authority = RULIB)
internal member
Name
(type = personal)
NamePart
(type = family)
Hsu
NamePart
(type = given)
Shu-Chan
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Shu-Chan Hsu
Affiliation
Advisory Committee
Role
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(authority = RULIB)
internal member
Name
(type = personal)
NamePart
(type = family)
Gallo
NamePart
(type = given)
Gianluca
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Gianluca Gallo
Affiliation
Advisory Committee
Role
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(authority = RULIB)
outside member
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Rutgers University
Role
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(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
OriginInfo
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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
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Carboxypeptidase E (CPE) is a member of the M14 metallocarboxypeptidases family and is responsible for the proteolytic processing of peptide intermediates in endocrine cells and neurons. The importance of CPE in the nervous system has been elucidated in recent years. CPE-/- mice display a variety of neuronal deficits, including abnormal dendritic structure, spine morphology, and degeneration and deficits in learning and memory. It remains unclear whether and how CPE may contribute to neurodevelopment in addition to its role in prohormone processing, sorting, and transport. In this dissertation, I show that the level of CPE expression in mouse brain increases during embryonic and early postnatal development, and I demonstrate that it is enriched in and expressed throughout neurons. By overexpressing or knocking down CPE in vivo using the in utero electroporation technique, I find that CPE is required for proper cortical neuron migration. In hippocampal neuronal cultures, both overexpression and knockdown of CPE result in decreased dendrite branching, indicating that a balance of CPE protein level is required for proper dendrite morphogenesis. Importantly, I report that the interaction between the CPE carboxyl terminus and p150Glued is critical for regulation of the subcellular localization of p150(Glued), which may in turn affect the stability and dynamics of microtubule networks and may be responsible for the effects seen from CPE overexpression on dendrite morphology and neuronal migration. In addition, I identify a novel function for CPE in regulating tubulin polyglutamylation and show that the zinc-binding motif of CPE is required to mediate this activity. The role of CPE-mediated tubulin polyglutamylation in neuronal migration and dendrite branching is also examined, and my results show that this activity is not involved in regulation of these processes. Together, this study shows that CPE and its interactor, p150(Glued), are important players in neurodevelopment. Moreover, the zinc-binding motif of CPE and its function in regulating tubulin polyglutamylation play distinctive roles than does the CPE carboxyl terminus during early brain development.
Subject
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Topic
Cell and Developmental Biology
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Title
Rutgers University Electronic Theses and Dissertations
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Identifier
ETD_8370
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electronic resource
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application/pdf
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text/xml
Extent
1 online resource (ix, 132 p. : ill.)
Note
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Ph.D.
Note
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Includes bibliographical references
Subject
(authority = ETD-LCSH)
Topic
Carboxypeptidases
Note
(type = statement of responsibility)
by Chen Liang
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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
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doi:10.7282/T3GM8BFN
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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
Liang
GivenName
Chen
Role
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RightsEvent
Type
Permission or license
DateTime
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2017-09-20 12:28:04
AssociatedEntity
Name
Chen Liang
Role
Copyright holder
Affiliation
Rutgers University. School of Graduate Studies
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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.
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DateTime
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2017-10-31
DateTime
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2019-10-31
Type
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Detail
Access to this PDF has been restricted at the author's request. It will be publicly available after October 31st, 2019.
Copyright
Status
Copyright protected
Availability
Status
Open
Reason
Permission or license
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windows xp
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2018-01-30T15:22:10
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