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Protein modification in plant innate immunity Goritschnig, Sandra
Abstract
Plant diseases cause major crop losses worldwide. Crop protection strategies enhancing the plants' own defence mechanisms could be a sustainable solution to ensure future food supply. This thesis describes my research effort to better understand the innate defence mechanisms in plants. Specific resistance responses towards invading pathogens are mediated by Resistance (R) proteins. They recognize pathogen-derived molecules and activate signalling cascades, initiating physiological responses to limit pathogen spread in infected cells while minimizing harmful effects on the rest of the plant. We use the unique gain-of-function R gene snd as a tool to identify components of resistance signalling in Arabidopsis thaliana. In a screen for suppressors of snc7-mediated constitutive resistance, we identified a number of modifier of snd (mos) mutants. My thesis focuses on the identification and characterization of mos5 and mos8. Both mutations partially suppress sndassociated morphological phenotypes and revert susceptibility to virulent pathogens to wild type levels. mos5 contains a deletion in one of two ubiquitin activating enzyme genes in Arabidopsis. The mutation in mos5 lies in a putative binding domain, potentially disrupting interaction with downstream ubiquitin acceptors. The mos5 single mutant displays enhanced susceptibility to virulent bacteria, as well as to bacteria carrying the effector protease AvrRpt2, indicating a role of ubiquitination in both specific and basal resistance. A mutation in the mos5 homolog UBA2 does not affect resistance, however, a double mutant mos5 uba2 is lethal, indicating that the two genes are partially redundant. mos8 is allelic to enhanced response to abscisic acid 1 (eral), which encodes the beta subunit of protein farnesyltransferase. Mutations in the gene are known to affect development and abscisic acid signalling. mos8 displays enhanced susceptibility to virulent and avirulent pathogens and acts additively with NPR1. Defects in geranylgeranylation, a protein modification similar to farnesylation, do not affect resistance responses against virulent or avirulent pathogens. Taken together, my data reveals the importance of post-translational modification of yet to be identified regulatory proteins in plant innate immunity. Further research will aim at unravelling the mechanisms by which mos5 and mos8 affect resistance signalling.
Item Metadata
Title |
Protein modification in plant innate immunity
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Creator | |
Publisher |
University of British Columbia
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Date Issued |
2006
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Description |
Plant diseases cause major crop losses worldwide. Crop protection
strategies enhancing the plants' own defence mechanisms could be a sustainable
solution to ensure future food supply. This thesis describes my research effort to
better understand the innate defence mechanisms in plants.
Specific resistance responses towards invading pathogens are mediated by
Resistance (R) proteins. They recognize pathogen-derived molecules and activate
signalling cascades, initiating physiological responses to limit pathogen spread in
infected cells while minimizing harmful effects on the rest of the plant.
We use the unique gain-of-function R gene snd as a tool to identify
components of resistance signalling in Arabidopsis thaliana. In a screen for
suppressors of snc7-mediated constitutive resistance, we identified a number of
modifier of snd (mos) mutants. My thesis focuses on the identification and
characterization of mos5 and mos8. Both mutations partially suppress sndassociated
morphological phenotypes and revert susceptibility to virulent
pathogens to wild type levels.
mos5 contains a deletion in one of two ubiquitin activating enzyme genes in
Arabidopsis. The mutation in mos5 lies in a putative binding domain, potentially
disrupting interaction with downstream ubiquitin acceptors. The mos5 single
mutant displays enhanced susceptibility to virulent bacteria, as well as to bacteria
carrying the effector protease AvrRpt2, indicating a role of ubiquitination in both
specific and basal resistance. A mutation in the mos5 homolog UBA2 does not
affect resistance, however, a double mutant mos5 uba2 is lethal, indicating that the
two genes are partially redundant.
mos8 is allelic to enhanced response to abscisic acid 1 (eral), which
encodes the beta subunit of protein farnesyltransferase. Mutations in the gene are
known to affect development and abscisic acid signalling. mos8 displays enhanced
susceptibility to virulent and avirulent pathogens and acts additively with NPR1.
Defects in geranylgeranylation, a protein modification similar to farnesylation, do
not affect resistance responses against virulent or avirulent pathogens. Taken together, my data reveals the importance of post-translational
modification of yet to be identified regulatory proteins in plant innate immunity.
Further research will aim at unravelling the mechanisms by which mos5 and mos8
affect resistance signalling.
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Genre | |
Type | |
Language |
eng
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Date Available |
2011-01-27
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Provider |
Vancouver : University of British Columbia Library
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Rights |
For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use.
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DOI |
10.14288/1.0100388
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URI | |
Degree | |
Program | |
Affiliation | |
Degree Grantor |
University of British Columbia
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Campus | |
Scholarly Level |
Graduate
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Aggregated Source Repository |
DSpace
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Rights
For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use.