| dc.description.abstracteng | Activation of the plant immune system after pathogen attack involves massive transcriptional reprogramming. In Arabidopsis thaliana, clade I TGA transcription factors (TFs) TGA1 and TGA4 have been shown to contribute to defense responses against the virulent biotrophic bacterial pathogen Pseudomonas syringae pv. maculicola ES4326 (Psm ES4326). Here, I report that the tga14 double mutant is also more susceptible towards the avirulent strain Pseudomonas syringae pv. tomato avrRPS4 (Pst avrRPS4). When acting within this signaling cascade, which is activated through the plant immune receptor RPS4, clade I TGA TFs function downstream of EDS1 (ENHANCED DISEASE SUSCEPTIBILTY1) and downstream of the plant defense hormone salicylic acid (SA). However, they function independently from NPR1 (NONEXPRESSOR OF PATHOGENESIS-RELATED GENES 1), a transcriptional co-activator of clade II TGA factors within the SA-dependent defense response systemic acquired resistance (SAR). Microarray analysis unraveled that EDS/SA-activated genes were less expressed in mock-infected tga14 plants as compared to mock-infected wildtype plants. However, these differences disappeared after infection with Pst avrRPS4. It is hypothesized that clade I TGA factors might be necessary for the early induction of defense genes, when SA levels are low, whereas at later stages, when SA levels increase, other transcription factors take over.
Furthermore, microarray analysis revealed that clade I TGA TFs are positive regulators of ROXY9 and negative regulators of ROXY11, ROXY12, ROXY13, and ROXY15. ROXYs are plant-specific glutaredoxin-like proteins that are known to interact with TGA TFs. Previous studies had reported that critical cysteines in TGA1 and potentially TGA4 form an internal disulfide bridge, which is reduced in SA-treated plants. Therefore ROXYs are candidate proteins that might transfer the required electrons from glutathione. In this thesis, a direct influence of ROXY9 on the redox state of TGA1 or TGA4 could not be shown. In addition, the in vivo importance of these cysteines could not be demonstrated in vivo because 35S:TGA1 constructs failed to complement the tga14 phenotype. Pathogen assays performed with ROXY9 RNAi lines turned out to be too variable to answer the question whether ROXY9 has an influence on avrRPS-triggered resistance. Ectopic expression of ROXY9 leads to reduced plant growth. Since this effect depends on the presence of clade I TGA TFs, it is concluded that ROXY9 influences the activity of TGA TFs. | de |