|dc.description.abstract||Arabidopsis thaliana is an established model plant system for studying plantpathogen
interactions. The knowledge garnered from examining the mechanism of
induced disease resistance in this model system can be applied to eliminate the cost and
danger associated with current means of crop protection.
A specific defense pathway, known as systemic acquired resistance (SAR),
involves whole plant protection from a wide variety of bacterial, viral and fungal
pathogens and remains induced weeks to months after being triggered. The ability of
Arabidopsis to mount SAR depends on the accumulation of salicylic acid (SA), the NPRI
(non-expressor of pathogenesis related gene 1) protein and the expression of a subset of
pathogenesis related (PR) genes. NPRI exerts its effect in this pathway through
interaction with a closely related class of bZIP transcription factors known as TGA
factors, which are named for their recognition of the cognate DNA motif TGACG.
We have discovered that one of these transcription factors, TGA2, behaves as a
repressor in unchallenged Arabidopsis and acts to repress NPRI-dependent activation of
PRJ. TGA1, which bears moderate sequence similarity to TGA2, acts as a transcriptional
activator in unchallenged Arabidopsis, however the significance of this activity is
unclear. Once SAR has been induced, TGAI and TGA2 interact with NPRI to form
complexes that are capable of activating transcription. Curiously, although TGAI is
capable of transactivating, the ability of the TGAI-NPRI complex to activate
transcription results from a novel transactivation domain in NPRI. This transactivation
domain, which depends on the oxidation of cysteines 521 and 529, is also responsible for
the transactivation ability of the TGA2-NPRI complex. Although the exact mechanism preventing TGA2-NPRI interaction in
unchallenged Arabidopsis is unclear, the regulation of TGAI-NPRI interaction is based
on the redox status of cysteines 260 and 266 in TGAl. We determined that a
glutaredoxin, which is an enzyme capable of regulating a protein's redox status, interacts
with the reduced form of TGAI and this interaction results .in the glutathionylation of
TGAI and a loss of interaction with NPRl.
Taken together, these results expand our understanding of how TGA transcription
factors and NPRI behave to regulate events and gene expression during SAR.
Furthermore, the regulation of the behavior of both TGAI and NPRI by their redox
status and the involvement of a glutaredoxin in modulating TGAI-NPRI interaction
suggests the redox regulation of proteins is a general mechanism implemented in SAR.||en_US