Staff View
Exploring the function of TRF-1, a tumor necrosis factor (TNF) receptor associated factor (TRAF) in C. elegans polycystin-expressing sensory neurons

Descriptive

TitleInfo
Title
Exploring the function of TRF-1, a tumor necrosis factor (TNF) receptor associated factor (TRAF) in C. elegans polycystin-expressing sensory neurons
Name (type = personal)
NamePart (type = family)
Santiago-Martinez
NamePart (type = given)
Dianaliz
NamePart (type = date)
1985-
DisplayForm
Dianaliz Santiago-Martinez
Role
RoleTerm (authority = RULIB)
author
Name (type = personal)
NamePart (type = family)
Barr
NamePart (type = given)
Maureen M
DisplayForm
Maureen M Barr
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
chair
Name (type = personal)
NamePart (type = family)
Rongo
NamePart (type = given)
Christopher
DisplayForm
Christopher Rongo
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
internal member
Name (type = personal)
NamePart (type = family)
Grant
NamePart (type = given)
Barth
DisplayForm
Barth Grant
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)
2013
DateOther (qualifier = exact); (type = degree)
2013-01
Place
PlaceTerm (type = code)
xx
Language
LanguageTerm (authority = ISO639-2b); (type = code)
eng
Abstract (type = abstract)
TRAFs are adaptor molecules that function mainly in the immune system. Mammals have seven TRAFs that share a conserved C-terminal domain. The C. elegans genome encodes two TRAF genes, trf-1 and trf-2 (Y110A7A.2). In humans, mutations in the polycystin-1 (PC-1) or polycystin-2 (PC-2) ciliary mechanosensory complex cause ADPKD. In C. elegans, the polycystins LOV-1 and PKD-2 localize to cilia and are required for male sensory behaviors. We find that trf-1 is co-expressed with pkd-2 in the male specific CEM, RnB, and HOB neurons and is required for male mating behaviors. We are interested in exploring a potential connection between immune recognition and mate recognition. We examined the mating behavior of mutant males defective in the Toll pathway including tol-1 and ikb-1. We performed leaving, retention, response, and vulva location (Lov) behavior assays. Like pkd-2 mutants, trf-1(nr2014) mutant males have response and Lov defects. In contrast, tol-1 and ikb-1 are like the wild-type. trf-1 and pkd-2 males are leaving assay (Las) defective, whereas tol-1 is Las but statistically different from pkd-2 and trf-1. ikb-1 males are not Las. All mutant strains are normal for the retention assay, indicating that these males can sense the presence of a mate. We conclude that trf-1 acts like pkd-2, suggesting they function in a similar pathway. The other TRAF gene, trf-2, is also mating defective and seems to act in the same pathway as trf-1. trf-1 and trf-2 act non-redundantly, since the double mutant does not yield a stronger phenotype. To ascertain the site of TRF-1 action, we generated transgenic animals expressing TRF-1::GFP. TRF-1::GFP localizes to cell bodies, dendrites and axons of CEM, HOB and RnB neurons. TRF-1::GFP is detectable in sensory cilia. The mating defects were partially rescued in the mutant. Genetic interactions between TRF-1 and components of the C. elegans PKD pathway (LOV-1, PKD-2, and KLP-6) showed no interaction in yeast two-hybrid experiments. Interestingly, TRF-1 showed interaction with EBAX-1/PQN-55, a substrate recognition subunit for cullin based E3 ligase complex. Ebax-1/pqn-55 males were also shown to be response and location of vulva defective. pqn-55 may act in the PKD pathway as well.
Subject (authority = RUETD)
Topic
Neuroscience
RelatedItem (type = host)
TitleInfo
Title
Rutgers University Electronic Theses and Dissertations
Identifier (type = RULIB)
ETD
Identifier
ETD_4507
PhysicalDescription
Form (authority = gmd)
electronic resource
InternetMediaType
application/pdf
InternetMediaType
text/xml
Extent
viii, 46 p. : ill.
Note (type = degree)
M.S.
Note (type = bibliography)
Includes bibliographical references
Note (type = statement of responsibility)
by Dianaliz Santiago-Martínez
Subject (authority = ETD-LCSH)
Topic
Tumor necrosis factor--Receptors
Subject (authority = ETD-LCSH)
Topic
Caenorhabditis elegans--Sexual behavior
Identifier (type = hdl)
http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000067831
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/T31V5CPF
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
Santiago-Martinez
GivenName
Dianaliz
Role
Copyright Holder
RightsEvent
Type
Permission or license
DateTime (encoding = w3cdtf); (qualifier = exact); (point = start)
2013-01-14 10:46:34
AssociatedEntity
Name
Dianaliz Santiago-Martinez
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.
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 8.4.8
Rutgers University Libraries - Copyright ©2022