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The novel RNA methylcytosine hydroxylase Tet in Drosophila and its requirement in neurons and muscles

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TitleInfo
Title
The novel RNA methylcytosine hydroxylase Tet in Drosophila and its requirement in neurons and muscles
Name (type = personal)
NamePart (type = family)
Wang
NamePart (type = given)
Fei
NamePart (type = date)
1989-
DisplayForm
Fei Wang
Role
RoleTerm (authority = RULIB)
author
Name (type = personal)
NamePart (type = family)
Steward
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Ruth
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Ruth Steward
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Advisory Committee
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chair
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Irvine
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Kenneth
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Kenneth Irvine
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Advisory Committee
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internal member
Name (type = personal)
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Zaratiegui
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Mikel
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Mikel Zaratiegui
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Advisory Committee
Role
RoleTerm (authority = RULIB)
internal member
Name (type = personal)
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Gartenberg
NamePart (type = given)
Marc
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Marc Gartenberg
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Advisory Committee
Role
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outside member
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Rutgers University
Role
RoleTerm (authority = RULIB)
degree grantor
Name (type = corporate)
NamePart
School of Graduate Studies
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school
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Text
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theses
OriginInfo
DateCreated (qualifier = exact)
2017
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2017-10
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2017
Place
PlaceTerm (type = code)
xx
Language
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eng
Abstract (type = abstract)
The TET (Ten-eleven translocation) 1, 2 and 3 proteins have been shown to function as DNA hydroxymethylases in vertebrates and their requirements have been documented extensively. We show that in Drosophila hydroxymethylcytosine preferentially marks polyadenylated RNAs and is deposited by Tet. Due to the lack of Cytosine methylation in DNA, Drosophila serves as an ideal model to study the biological function of 5hmrC. We maped the transcriptome-wide hydroxymethylation landscape, revealing hydroxymethylcytosine in the transcripts of many genes, notably in coding sequences, and identified consensus sites for hydroxymethylation. We found that RNA hydroxymethylation may favor mRNA translation. We show that Tet is essential for viability as Tet complete loss-of-function animals die at the late pupal stage. We also characterized the temporal and spatial expression and requirement of Tet throughout Drosophila development. Tet is highly expressed in neuronal tissues and at more moderate levels in somatic muscle precursors in embryos and larvae. Depletion of Tet in muscle precursors at early embryonic stages leads to defects in larval locomotion and late pupal lethality. Although Tet knock-down in neuronal tissue does not cause lethality, Tet is essential for neuronal function during development and affects locomotion in larvae and adults, as well as the circadian rhythm of adult flies. Further, we report the function of Tet in ovarian morphogenesis. Together, our findings provide basic insights into the biological function of 5hmrC, a modification that is likely also regulated by Tet proteins in other species, and may illuminate observed neuronal and muscle phenotypes observed in vertebrates.
Subject (authority = RUETD)
Topic
Cell and Developmental Biology
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Title
Rutgers University Electronic Theses and Dissertations
Identifier (type = RULIB)
ETD
Identifier
ETD_8367
PhysicalDescription
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electronic resource
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application/pdf
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text/xml
Extent
1 online resource (viii, 102 p. : ill.)
Note (type = degree)
Ph.D.
Note (type = bibliography)
Includes bibliographical references
Subject (authority = ETD-LCSH)
Topic
RNA
Note (type = statement of responsibility)
by Fei Wang
RelatedItem (type = host)
TitleInfo
Title
School of Graduate Studies Electronic Theses and Dissertations
Identifier (type = local)
rucore10001600001
Location
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NjNbRU
Identifier (type = doi)
doi:10.7282/T3VT1W8V
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
Wang
GivenName
Fei
Role
Copyright Holder
RightsEvent
Type
Permission or license
DateTime (encoding = w3cdtf); (qualifier = exact); (point = start)
2017-09-19 16:22:42
AssociatedEntity
Name
Fei Wang
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.
RightsEvent
DateTime (encoding = w3cdtf); (qualifier = exact); (point = start)
2017-10-31
DateTime (encoding = w3cdtf); (qualifier = exact); (point = end)
2019-10-31
Type
Embargo
Detail
Access to this PDF has been restricted at the author's request. It will be publicly available after October 31st, 2019.
Copyright
Status
Copyright protected
Availability
Status
Open
Reason
Permission or license
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2017-09-25T16:04:13
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2017-09-25T16:04:13
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