Staff View
Plexin-A4 receptor regulates dendrite morphogenesis in response to Class 3 Semaphorin 3A signaling in mouse pyramidal neurons

Descriptive

TitleInfo
Title
Plexin-A4 receptor regulates dendrite morphogenesis in response to Class 3 Semaphorin 3A signaling in mouse pyramidal neurons
Name (type = personal)
NamePart (type = family)
Peng
NamePart (type = given)
Sheng-Shiang (Anson)
NamePart (type = date)
1984-
DisplayForm
Sheng-Shiang (Anson) Peng
Role
RoleTerm (authority = RULIB)
author
Name (type = personal)
NamePart (type = family)
Tran
NamePart (type = given)
Tracy
DisplayForm
Tracy Tran
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
chair
Name (type = personal)
NamePart (type = family)
Haspel
NamePart (type = given)
Gal
DisplayForm
Gal Haspel
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
internal member
Name (type = personal)
NamePart (type = family)
Maurel
NamePart (type = given)
Patrice
DisplayForm
Patrice Maurel
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
internal member
Name (type = corporate)
NamePart
Rutgers University
Role
RoleTerm (authority = RULIB)
degree grantor
Name (type = corporate)
NamePart
Graduate School - Newark
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)
The formation of a complicate nervous system requires precise navigation and elaboration for growth cone and dendrites to connect to their target. During development, guidance molecules and receptors control the majority of the circuitry events, including promotion or inhibition of neurite growth. Semphorin 3A, a secreted Class 3 Semaphorin member, is well known for its chemorepellent function on growth cone mediated by the Neuropilin1/PlexinA4 holoreceptor complex. Recently, it has been shown to have opposite cellular responses in promoting dendrite growth and branching in mouse cortical pyramidal neurons (1, 2). However, the mechanism underlying how Semaphorin 3A/Neuropilin1/Plexin-A4 signaling regulates dendrite elaboration is unclear. Here, I have shown the importance and function of three distinct domains in the cytoplasmic region of the signaling transducing receptor of Semaphorin 3A, Plexin-A4, in regulating cortical neuron dendritic morphology. Both the C1 and H/RBD domains were found to be sufficient to trigger cortical pyramidal neuron dendrite elaboration, while the C2 domain was not necessary for dendrites growth and branching. Using biochemical and molecular methods in combination with in vitro assays, I found and demonstrated that the Rho-GEF, FARP2 associates with PlexinA4 and mediates dendritic elaboration in primary cortical neurons following the ligand, Semaphorin 3A activation of the signaling pathway. In addition, I demonstrated that Plexin-A4 extracellular domains could interact with its co-receptor Neuropilin1, independent of the ligand Semaphorin 3A. Therefore, the extracellular Semaphorin domain may play a role in preventing Plexin-A4 activation, consistent with previous studies (3, 4). Previously, another member of the Type A Plexin receptor, Plexin-A3, was shown to play a key role in inhibiting cortical neuron dendritic spine morphogenesis in vivo (2). However, the mechanism of how Plexin-A3 signals to restrain spine formation is unknown. I have generated an array of Plexin-A3 cytoplasmic deletion mutant constructs, analogous to the Plexin-A4 deletion mutants used for this study for future studies in investigating cortical neuron dendritic spine morphology. These molecular tools that I have developed will be useful for researchers to investigate the intracellular signaling mechanisms of Semaphorin signaling in regulating neuron morphology. Taken together, my findings provide new insights to Plexin-A4 signaling, in particular, highlighting distinct intracellular domains and downstream effectors required for promoting dendritic morphology.
Subject (authority = RUETD)
Topic
Biology
RelatedItem (type = host)
TitleInfo
Title
Rutgers University Electronic Theses and Dissertations
Identifier (type = RULIB)
ETD
Identifier
ETD_5962
PhysicalDescription
Form (authority = gmd)
electronic resource
InternetMediaType
application/pdf
InternetMediaType
text/xml
Extent
1 online resource (x, 84 p. : ill.)
Note (type = degree)
M.S.
Note (type = bibliography)
Includes bibliographical references
Note (type = vita)
Includes vita
Subject (authority = ETD-LCSH)
Topic
Neurons--Growth
Subject (authority = ETD-LCSH)
Topic
Semaphorins
Subject (authority = ETD-LCSH)
Topic
Dendrites
Note (type = statement of responsibility)
by Sheng-Shiang (Anson) Peng
RelatedItem (type = host)
TitleInfo
Title
Graduate School - Newark Electronic Theses and Dissertations
Identifier (type = local)
rucore10002600001
Location
PhysicalLocation (authority = marcorg); (displayLabel = Rutgers, The State University of New Jersey)
NjNbRU
Identifier (type = doi)
doi:10.7282/T3TF0001
Genre (authority = ExL-Esploro)
ETD graduate
Back to the top

Rights

RightsDeclaration (ID = rulibRdec0006)
The author owns the copyright to this work.
RightsHolder (type = personal)
Name
FamilyName
Peng
GivenName
Sheng-Shiang (Anson)
Role
Copyright Holder
RightsEvent
Type
Permission or license
DateTime (encoding = w3cdtf); (qualifier = exact); (point = start)
2014-10-01 14:40:40
AssociatedEntity
Name
Sheng-Shiang (Anson) Peng
Role
Copyright holder
Affiliation
Rutgers University. Graduate School - Newark
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.
Copyright
Status
Copyright protected
Availability
Status
Open
Reason
Permission or license
Back to the top

Technical

RULTechMD (ID = TECHNICAL1)
ContentModel
ETD
OperatingSystem (VERSION = 5.1)
windows xp
Back to the top
Version 8.3.13
Rutgers University Libraries - Copyright ©2021