Redox-active cysteines in TGACG-BINDING FACTOR 1 (TGA1) do not play a role in salicylic acid- or pathogen-induced expression of TGA1-regulated target genes in Arabidopsis thaliana

Abstract

SummarySalicylic acid (SA) is an important signaling molecule of the plant immune system.SA biosynthesis is indirectly modulated by the closely related transcription factors TGA1 (TGACG-BINDING FACTOR 1) and TGA4. They activate expression of SARD1 (SYSTEMIC ACQUIRED RESISTANCE DEFICIENT1), the gene product of which regulates the key SA biosynthesis gene ICS1 (ISOCHORISMATE SYNTHASE 1).Since TGA1 interacts with the SA receptor NPR1 (NON EXPRESSOR OF PATHOGENESIS-RELATED GENES 1) in a redox-dependent manner and since the redox state of TGA1 is altered in SA-treated plants, TGA1 was assumed to play a role in the NPR1-dependent signaling cascade. Here we identified 193 out of 2090 SA-induced genes that require TGA1/TGA4 for maximal expression after SA treatment. One robustly TGA1/TGA4-dependent gene encodes for the SA hydroxylase DLO1 (DOWNY MILDEW RESISTANT 6-LIKE OXYGENASE 1) suggesting an additional regulatory role of TGA1/TGA4 in SA catabolism.Expression of TGA1/TGA4-dependent genes in mock/SA-treated or Pseudomonas-infected plants was rescued in the tga1 tga4 double mutant after introduction of a mutant genomic TGA1 fragment encoding a TGA1 protein without any cysteines. Thus, the functional significance of the observed redox modification of TGA1 in SA-treated tissues has remained enigmatic.SIGNIFICANCE STATEMENTPrevious findings demonstrating a redox-dependent interaction between transcription factor TGA1 and NPR1 attracted considerable attention. Here we show that TGA1 can act in the NPR1- and SA-dependent signaling cascade, but that its SA-regulated redox-active cysteines do not affect its function in this process.