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Hippo signaling in regeneration and neoplastic tumors

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TitleInfo
Title
Hippo signaling in regeneration and neoplastic tumors
Name (type = personal)
NamePart (type = family)
Sun
NamePart (type = given)
Gongping
NamePart (type = date)
1987-
DisplayForm
Gongping Sun
Role
RoleTerm (authority = RULIB)
author
Name (type = personal)
NamePart (type = family)
Irvine
NamePart (type = given)
Kenneth D.
DisplayForm
Kenneth D. Irvine
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
chair
Name (type = personal)
NamePart (type = family)
Padgett
NamePart (type = given)
Richard
DisplayForm
Richard Padgett
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
internal member
Name (type = personal)
NamePart (type = family)
Mckim
NamePart (type = given)
Kim
DisplayForm
Kim Mckim
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
internal member
Name (type = personal)
NamePart (type = family)
Karantza
NamePart (type = given)
Vassiliki
DisplayForm
Vassiliki Karantza
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)
2014-05
Place
PlaceTerm (type = code)
xx
Language
LanguageTerm (authority = ISO639-2b); (type = code)
eng
Abstract (type = abstract)
Hippo signaling controls organ size during development from Drosophila to humans. It limits tissue growth through regulation of cell proliferation and apoptosis. Deregulation of Hippo signaling leads to tissue overgrowth and tumor formation. An important characteristic of Hippo signaling is its connection to other pathways, through which Hippo signaling plays an indispensable role in diverse biological processes. We found, in addition to regulating growth during development, Hippo signaling regulates growth during regeneration. The growth suppression effect of Hippo signaling is through inhibition of a transcriptional co-activator Yorkie (Yki). Yki can promote cell proliferation and suppress apoptosis. Using the Drosophila wing imaginal disc, a mono-layered epithelial tissue, as a model, we found Yki is activated in the wing discs in response to apoptosis induction. Yki remains active over the entire wing disc regeneration. Yki activation during regeneration requires c-Jun N-terminal kinase (JNK). JNK activation of Yki is independent of cell death, and through a Hippo pathway component, Jub (a fly Ajuba LIM domain protein). Both Yki and Jub are required for wing regeneration. We also observed activation of Yki in the neoplastic tumors caused by disruption of epithelial apical-basal polarity. The growth of the neoplastic tumors is JNK-dependent. Like in regeneration, Yki activation in the neoplastic tumors also requires regulation of Jub by JNK. Reduction of Yki or Jub level suppresses tumor growth. Our work identified Jnk regulation of Hippo signaling as an important mechanism to drive the stress-responsive tissue growth, and established Jub and Yki as stress-responsive molecules. JNK regulation of Yki is also conserved in mammalian cells. Using cultured epithelial cell lines, we found manipulation of JNK activity affects the activity of YAP (the mammalian homolog of Yki), like what we observed in flies. And JNK influences the binding of the mammalian Ajuba proteins to LATS (the mammalian homolog of Wts, a core kinase that suppresses Yki activity) through a phosphorylation-dependent mechanism. Ajuba proteins may serve as a hub connecting multiple pathways to the Hippo pathway as the binding between Ajuba proteins and LATS can also be regulated by other signaling pathways. The activity of Ajuba proteins may depend on their conformation.
Subject (authority = RUETD)
Topic
Cell and Developmental Biology
RelatedItem (type = host)
TitleInfo
Title
Rutgers University Electronic Theses and Dissertations
Identifier (type = RULIB)
ETD
Identifier
ETD_5338
PhysicalDescription
Form (authority = gmd)
electronic resource
InternetMediaType
application/pdf
InternetMediaType
text/xml
Extent
xiv, 164 p. : ill.
Note (type = degree)
Ph.D.
Note (type = bibliography)
Includes bibliographical references
Note (type = statement of responsibility)
by Gongping Sun
Subject (authority = ETD-LCSH)
Topic
Regeneration (Biology)
Subject (authority = ETD-LCSH)
Topic
Growth--Regulation
Subject (authority = ETD-LCSH)
Topic
Neoplastic endocrine-like syndromes
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/T3BZ64CQ
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
Sun
GivenName
Gongping
Role
Copyright Holder
RightsEvent
Type
Permission or license
DateTime (encoding = w3cdtf); (qualifier = exact); (point = start)
2014-02-27 15:20:24
AssociatedEntity
Name
Gongping Sun
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)
2014-05-31
DateTime (encoding = w3cdtf); (qualifier = exact); (point = end)
2016-05-30
Type
Embargo
Detail
Access to this PDF has been restricted at the author's request. It will be publicly available after May 30th, 2016.
Copyright
Status
Copyright protected
Availability
Status
Open
Reason
Permission or license
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RULTechMD (ID = TECHNICAL1)
ContentModel
ETD
OperatingSystem (VERSION = 5.1)
windows xp
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