S-nitrosothiols and reactive oxygen species in plant disease resistance and development
dc.contributor.advisor
Loake, Gary
en
dc.contributor.advisor
Goodrich, Justin
en
dc.contributor.author
Brzezek, Kerstin
en
dc.contributor.sponsor
Darwin Trust of Edinburgh
en
dc.date.accessioned
2014-11-17T16:02:44Z
dc.date.available
2014-11-17T16:02:44Z
dc.date.issued
2014-06-28
dc.description.abstract
Nitric oxide (NO) as well as reactive oxygen species (ROS) play an important
role in defence signalling in plants. After successful recognition of an invading
pathogen, an increase in ROS occurs, the ’oxidative burst’; and a ’nitrosative
burst’ is also observed. This leads to the induction of defence responses, including
the ’hypersensitive response’ (HR), a form of programmed cell death.
A balanced production of hydrogen peroxide and NO is crucial for HR induction.
In a process called S-nitrosylation, NO can react with cysteine thiols
to form S-nitrosothiols, or react with glutathione to form S-nitrosoglutathione
(GSNO). The enzyme GNSO reductase (GSNOR) indirectly regulates SNO
levels by turning over GNSO. The Arabidopsis thaliana T-DNA insertion mutant
atgsnor1-3 shows a complete loss of GNSOR activity and has drastically
increased SNO levels, resulting in stunted growth, loss of apical dominance,
increased HR, loss of salicylic acid (SA) accumulation and increased susceptibility
to avirulent, virulent and non-host pathogens. Two recessive and allelic
EMS suppressor mutants in the atgsnor1-3 background were isolated, which
showed mostly wild type growth. The mutations were identified by map-based
cloning as two different point mutations in At1g20620 or CAT3, one of three
catalase genes in Arabidopsis. Catalases break down hydrogen peroxide, with CAT2 being the major catalase in Arabidopsis. All three catalases are structurally
very similar, but show temporal and spatial differences in their expression
patterns. The suppressor mutants recovered apical dominance, and
partially recovered disease resistance to avirulent pathogens, but were still susceptible
to virulent pathogens and showed decreased SA levels. The suppressor
mutants showed wild type HR in response to different avirulent bacteria.
Interestingly,
loss-of-function of the other catalase genes as well as loss-of-function
of other redox-related genes did not restore apical dominance of atgnsor1-3
plants. This effect seems to be highly specific to CAT3, possibly because of its
expression pattern or its expression levels. Further research is needed to fully
understand the mechanisms at work here, but these results certainly seem to
show a direct connection between redox signalling and S-nitrosylation.
en
dc.identifier.uri
http://hdl.handle.net/1842/9653
dc.language.iso
en
dc.publisher
The University of Edinburgh
en
dc.subject
S-nitrosylation
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dc.subject
plant defence
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dc.subject
reactive oxygen species
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dc.title
S-nitrosothiols and reactive oxygen species in plant disease resistance and development
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dc.type
Thesis or Dissertation
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dc.type.qualificationlevel
Doctoral
en
dc.type.qualificationname
PhD Doctor of Philosophy
en
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