SnRK1-triggered switch of bZIP63 dimerization mediates the low-energy response in plants

Abstract

Metabolic adjustment to changing environmental conditions, particularly balancing of growth and defense responses, is crucial for all organisms to survive. The evolutionary conserved AMPK/Snf1/SnRK1 kinases are well-known metabolic master regulators in the low-energy response in animals, yeast and plants. They act at two different levels: by modulating the activity of key metabolic enzymes, and by massive transcriptional reprogramming. While the first part is well established, the latter function is only partially understood in animals and not at all in plants. Here we identified the Arabidopsis transcription factor bZIP63 as key regulator of the starvation response and direct target of the SnRK1 kinase. Phosphorylation of bZIP63 by SnRK1 changed its dimerization preference, thereby affecting target gene expression and ultimately primary metabolism. A bzip63 knock-out mutant exhibited starvation-related phenotypes, which could be functionally complemented by wild type bZIP63, but not by a version harboring point mutations in the identified SnRK1 target sites.DOI: http://dx.doi.org/10.7554/eLife.05828.001

Gene Regulation and Survival under Hypoxia Requires Starch Availability and Metabolism

“…The expression of the starvation-induced DIN6 gene always correlated with repression of ADH following an extended night treatment. Expression of DIN6 is under control of bZIP63 (Mair et al, 2015); however, neither the bzip63 mutant nor a bZIP63 overexpression line displayed any alteration of the expression of ADH (Fig. 9), thus ruling out this possible link.…”

“…The quintuple erfVII mutant (Marín-de la ) is a null mutant for RAP2.2, RAP2.3, RAP2.12, HRE1, HRE2, and a knockdown for RAP2.2 (Giuntoli et al, 2017b); a line constitutively expressing a version of the RAP2.12 protein that is also stable in air (35S:D-RAP2.12; Licausi et al, 2011); a line expressing GUS under the control of the PCO1 promoter (pPCO1:GUS; Weits et al, 2014); and a line overexpressing HRA1 . The bzip63 mutant and the bZIP63 overexpressor (35S:bZIP63) (Mair et al, 2015), two independent KIN10 overexpressor lines (OE1 KIN10 and OE2 KIN10) (Baena-González et al, 2007); the Arabidopsis SnRK1.1 dominant-negative mutant (SnRK1.1 K48M ; Cho et al, 2016); a line expressing RAP2.3 with an HA tag (35S:RAP2.3-HA; Gibbs et al, 2014).…”

Transitioning to the Next Phase: The Role of Sugar Signaling throughout the Plant Life Cycle

“…SnRK1 acts at least partially via activation of the C/S1 group of bZIP transcription factors (Baena-González et al, 2007). Recently, a mechanism for this activation has been described: By phosphorylation of the C-group bZIP63, SnRK1 promotes bZIP homo-and heterodimerization, for example, with S-group bZIPs (such as bZIP11) that are not themselves phosphorylated by SnRK1 (Mair et al, 2015). Similar to SnRK1, C/S1 group bZIP transcription factors, whose expression is controlled by Suc-induced repression of translation , are involved in reprogramming metabolism in response to low energy supply.…”

The Energy-Signaling Hub SnRK1 Is Important for Sucrose-Induced Hypocotyl Elongation

“…SnRK1 controls metabolic enzymes directly by protein phosphorylation (Baena-González and Sheen, 2008). It also regulates greater than 1000 transcripts in response to carbohydrate availability, for example by adjusting bZIP transcription factor activity (Baena-González et al, 2007;Smeekens et al, 2010;Delatte et al, 2011;Matiolli et al, 2011;Mair et al, 2015). Both SnRK1-and hexokinasemediated sugar signaling involve specific sugars functioning as signaling molecules that provide cellular information concerning sugar availability.…”