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Characterizing the role of mitochondria in the toxicity of trichothecenes produced by Fusarium graminearum
Descriptive
TitleInfo
Title
Characterizing the role of mitochondria in the toxicity of trichothecenes produced by Fusarium graminearum
Name
(type = personal)
NamePart
(type = family)
Bin Umer
NamePart
(type = given)
Mohamed Anwar
DisplayForm
Mohamed Anwar Bin Umer
Role
RoleTerm
(authority = RULIB)
author
Name
(type = personal)
NamePart
(type = family)
Tumer
NamePart
(type = given)
Nilgun
DisplayForm
Nilgun Tumer
Affiliation
Advisory Committee
Role
RoleTerm
(authority = RULIB)
chair
Name
(type = personal)
NamePart
(type = family)
Cohick
NamePart
(type = given)
Wendie
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Wendie Cohick
Affiliation
Advisory Committee
Role
RoleTerm
(authority = RULIB)
internal member
Name
(type = personal)
NamePart
(type = family)
Laskin
NamePart
(type = given)
Jeffrey
DisplayForm
Jeffrey Laskin
Affiliation
Advisory Committee
Role
RoleTerm
(authority = RULIB)
internal member
Name
(type = personal)
NamePart
(type = family)
Jin
NamePart
(type = given)
Shengkan
DisplayForm
Shengkan Jin
Affiliation
Advisory Committee
Role
RoleTerm
(authority = RULIB)
internal member
Name
(type = personal)
NamePart
(type = family)
Ivessa
NamePart
(type = given)
Andreas
DisplayForm
Andreas Ivessa
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)
2014-01
Place
PlaceTerm
(type = code)
xx
Language
LanguageTerm
(authority = ISO639-2b);
(type = code)
eng
Abstract
(type = abstract)
Fusarium graminearum is a toxigenic fungal pathogen infecting economically significant cereal crops. Trichothecenes are a large family of low molecular weight sesquiterpenoid mycotoxins synthesized by F. graminearum and other fungi and are among the most toxic compounds known to man. These mycotoxins and their producers are encountered worldwide in the environment as natural contaminants of cereal grains presenting a high food safety risk for humans and cattle and threaten the global food supply. Trichothecene mycotoxicosis was primarily associated with their inhibitory effects on translation. However, these highly stable toxins also inhibit other cellular processes which contribute to their toxicity. In this work, using yeast as a model organism, a genome wide approach has been applied to obtain a comprehensive understanding of the molecular mechanism of the type A and B trichothecene toxicity. Due to their prevalence and impact, T-2 toxin and diacetoxyscirpenol (DAS) are used as representative type A toxins while trichothecin (Tcin) and deoxynivalenol (DON) are used as representative type B toxins. The yeast knockout collection of nonessential genes was initially used to identify mutant strains that exhibited increased resistance or susceptibility to trichothecenes. This screening led to identification of the role of mitochondria during trichothecene toxicity. The largest group of mutants exhibiting resistance was affected in their mitochondrial functions. Mitochondrial translation was directly inhibited, independent of total translation, and the trichothecene-treated cells exhibited severe fragmentation of mitochondrial membrane. Furthermore, actively respiring cells with functional mitochondria were essential for trichothecene cytotoxicity suggesting a critical role for mitochondria. A large fraction of the highly susceptible strains exhibited very high levels of reactive oxygen species (ROS) upon trichothecene treatment. Antioxidants increased cell survival and reduced mitochondrial membrane damage in trichothecene-treated cells. The direct role for ROS in mediating trichothecene cytotoxicity was confirmed when two novel Arabidopsis nonspecific lipid transfer proteins that mediated resistance to trichothecenes in A. thaliana exhibited antioxidant property and rescued trichothecene-treated yeast cells. Rapamycin-induced mitophagy reduced ROS levels and increased survival in trichothecene-treated cells suggesting mitophagy as a novel prosurvival cellular mechanism during oxidative stress in trichothecene-treated cells.
Subject
(authority = RUETD)
Topic
Microbiology and Molecular Genetics
RelatedItem
(type = host)
TitleInfo
Title
Rutgers University Electronic Theses and Dissertations
Identifier
(type = RULIB)
ETD
Identifier
ETD_5305
PhysicalDescription
Form
(authority = gmd)
electronic resource
InternetMediaType
application/pdf
InternetMediaType
text/xml
Extent
xv, 171 p. : ill.
Note
(type = degree)
Ph.D.
Note
(type = bibliography)
Includes bibliographical references
Note
(type = statement of responsibility)
by Mohamed Anwar Bin Umer
Subject
(authority = ETD-LCSH)
Topic
Mitochondrial pathology
Subject
(authority = ETD-LCSH)
Topic
Fusarium
Subject
(authority = ETD-LCSH)
Topic
Yeast fungi--Biotechnology
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/T3QJ7FDJ
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
Bin Umer
GivenName
Mohamed Anwar
Role
Copyright Holder
RightsEvent
Type
Permission or license
DateTime
(encoding = w3cdtf);
(qualifier = exact);
(point = start)
2014-01-06 15:47:23
AssociatedEntity
Name
Mohamed Anwar Bin Umer
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
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Technical
RULTechMD
(ID = TECHNICAL1)
ContentModel
ETD
OperatingSystem
(VERSION = 5.1)
windows xp
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