Sweet connections, bZIP transcription factors and the regulation of metabolism in Arabidopsis

Abstract

bZIP transcription factors are part of an intricate signaling network connecting sugar signaling to metabolism (Figure 1.5). Many inputs and components of this system are known, but little is known on the actual function of bZIP transcription factors. In this thesis the function of bZIPs within this vital signaling network is studied. The model organism Arabidopsis thaliana was used to identify targets genes and metabolic effects of bZIP transcription factors. In chapter 2, target genes of bZIP11 are presented. Using transgenic plants in which the in vivo amount of the bZIP11 protein can be induced, in combination with global transcriptional profiling and further experimentation, bZIP11 is established as an inducer of the expression of hundreds of genes. Among the target genes of bZIP11 are ASN1 and the ProDH2 (At5g38710), linking bZIP, and thus sugar signaling, to amino acid metabolism. Many of the targets identified are previously known sugar regulated genes. In chapter 3, the effect of induced bZIP11 activity on metabolite levels is investigated using the same transgenic plant lines used to identify bZIP11 target genes. The effect on metabolite levels is studied using both targeted and unbiased approaches. It is concluded that bZIP11 induction causes metabolic reprogramming, as its overexpression has profound effects on amino acid levels as well as other metabolites. In chapter 4, the translational effects of specific bZIP dimers are characterized. The dimerization preferences of a number of bZIP transcription factors in planta are known (Ehlert et al., 2006a) Therefore, specific bZIPs were co-expressed in protoplasts, which were subjected to mRNA profiling experiments. From these experiments it can be concluded that different bZIP dimers have differential effects on target gene expression. Finally in chapter 5, the findings presented in this thesis will be briefly summarized and their implications discussed.