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Regulation of phospholipid synthesis in Saccharomyces cerevisiae by mRNA stability
Descriptive
TypeOfResource
Text
TitleInfo
(ID = T-1)
Title
Regulation of phospholipid synthesis in Saccharomyces cerevisiae by mRNA stability
Identifier
ETD_450
Identifier
(type = hdl)
http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000054797
Language
LanguageTerm
(authority = ISO639-2);
(type = code)
eng
Genre
(authority = marcgt)
theses
Subject
(ID = SBJ-1);
(authority = RUETD)
Topic
Food Science
Subject
(ID = SBJ-2);
(authority = ETD-LCSH)
Topic
Saccharomyces cerevisiae
Subject
(ID = SBJ-3);
(authority = ETD-LCSH)
Topic
Messenger RNA
Subject
(ID = SBJ-4);
(authority = ETD-LCSH)
Topic
RNA editing
Abstract
(type = abstract)
In the yeast Saccharomyces cerevisiae, the most abundant phospholipid phosphatidylcholine is synthesized by the complementary CDP-diacylglycerol and Kennedy pathways. Using a cki1D eki1D mutant defective in choline kinase and ethanolamine kinase, we examined the consequences of a block in the Kennedy pathway on the regulation of phosphatidylcholine synthesis by the CDP-diacylglycerol pathway. The cki1D eki1D mutant exhibited increases in the synthesis of phosphatidylserine, phosphatidylethanolamine and phosphatidylcholine via the CDP-diacylglycerol pathway. The increase in phospholipid synthesis correlated with increased activity levels of the CDP-diacylglycerol pathway enzymes phosphatidylserine synthase, phosphatidylserine decarboxylase, phosphatidylethanolamine methyltransferase, and phospholipid methyltransferase. However, other enzyme activities, including phosphatidylinositol synthase and phosphatidate phosphatase, were not affected in the cki1D eki1D mutant. For phosphatidylserine synthase, the enzyme catalyzing the committed step in the pathway, activity was regulated by increases in the levels of mRNA and protein. Decay analysis of CHO1 mRNA indicated that a dramatic increase in transcript stability was a major component responsible for the elevated level of phosphatidylserine synthase. We examined the decay pathway of CHO1 mRNA by analyzing the rates of transcript degradation in mutants defective in a specific mRNA decay pathway. When compared with the decay (t1/2 = 10-12 min) of the wild type control, the half-life of CHO1 mRNA was increased (t1/2 > 45 min) in the ccr4D, dcp1D, and xrn1D mutants defective in deadenylation, decapping, and 5’-to-3’ exonucleolytic degradation, respectively. The stability of CHO1 mRNA also increased in the ski4-1 mutant defective in the 3’-to-5’ exosome-mediated decay pathway. These results indicated that CHO1 mRNA in S. cerevisiae is degraded through the 5’-to-3’ and 3’-to-5’ decay pathways. We also found that CHO1 mRNA decay was defective in respiratory deficient mutants that were derived from wild type cells and from an eki1 D mutant. The respiratory inhibitor KCN caused a dose dependent increase in CHO1 mRNA stability. This increase in mRNA stability was recapitulated in a cox4D mutant defective in the cytochrome c oxidase enzyme. These results indicated that mitochondrial respiration was required for normal CHO1 mRNA decay.
PhysicalDescription
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electronic resource
Extent
xiii, 114 p. : ill.
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application/pdf
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text/xml
Note
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Ph.D.
Note
Includes abstract
Note
Vita
Note
(type = bibliography)
Includes bibliographical references
Note
(type = statement of responsibility)
by Hyeon-Son Choi
Name
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Choi
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Hyeon-Son
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author
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Hyeon-Son Choi
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NamePart
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Carman
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(type = given)
George M
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chair
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Advisory Committee
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George M Carman
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(type = family)
Mattews
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(type = given)
Karl R
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internal member
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Advisory Committee
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Karl R Mattews
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(ID = NAME-4);
(type = personal)
NamePart
(type = family)
Chikindas
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(type = given)
Mikhael L
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internal member
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Advisory Committee
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Mikhael L Chikindas
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(type = personal)
NamePart
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Martin
NamePart
(type = given)
Charles E
Role
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outside member
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Advisory Committee
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Charles E Martin
Name
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NamePart
Rutgers University
Role
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degree grantor
Name
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NamePart
Graduate School - New Brunswick
Role
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school
OriginInfo
DateCreated
(qualifier = exact)
2007
DateOther
(qualifier = exact);
(type = degree)
2007
Place
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(type = code)
xx
RelatedItem
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TitleInfo
Title
Rutgers University Electronic Theses and Dissertations
Identifier
(type = RULIB)
ETD
RelatedItem
(type = host)
TitleInfo
Title
Graduate School - New Brunswick Electronic Theses and Dissertations
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rucore19991600001
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NjNbRU
Identifier
(type = doi)
doi:10.7282/T3CJ8DFV
Genre
(authority = ExL-Esploro)
ETD doctoral
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Rights
RightsDeclaration
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(ID = rulibRdec0006)
The author owns the copyright to this work.
Copyright
Status
Copyright protected
Availability
Status
Open
Reason
Permission or license
RightsHolder
(ID = PRH-1);
(type = personal)
Name
FamilyName
Choi
GivenName
Hyeon-Son
Role
Copyright Holder
RightsEvent
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Type
Permission or license
DateTime
2007-09-27 13:49:33
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Name
Hyeon-Son Choi
Affiliation
Rutgers University. Graduate School - New Brunswick
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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.
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Technical
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ETD
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application/pdf
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application/x-tar
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768000
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