|
Description
|
Changes in water and nutrient availability, soil salinity and extreme temperatures, amongst others, generate signals in plants that need to be finely integrated with metabolic activity and development for optimal growth and survival [1]. One such signal is energy deficiency derived from impaired carbon assimilation and/or respiration in situations of stress, which triggers the activation of the highly conserved SnRK1 (Snf1-Related protein Kinase 1) protein kinases to restore homeostasis and elaborate adequate longer-term responses [2]. SnRK1s coordinate nutrient remobilization, growth, and storage and promote stress tolerance through the regulation of key biosynthetic enzymes and over a thousand genes [2, 3]. Accordingly, SnRK1 deficiency is associated with a diminished ability of plants to tolerate abiotic and biotic stress. In addition, SnRK1 has an impact on fundamental developmental processes, from seed maturation and germination to reproduction and senescence [2-6]. SnRK1s are the plant orthologs of the yeast Snf1 (Sucrose non fermenting 1) and mammalian AMPK (AMP-activated protein kinase). All of these systems require phosphorylation of a highly conserved T-loop residue for the activation of the kinase [3]. In mammalian cells energy deficiency is signaled through AMP binding to the AMPK complex, promoting its phosphorylation by upstream kinases and preventing its dephosphorylation by yet undefined phosphatases [7]. Clade A PP2Cs are well established repressors of the ABA pathway through their interaction with SnRK2s, more divergent members of the Snf1/AMPK/SnRK family and specific to plants [8, 9]. Arabidopsis contains 10 SnRK2s of which three, SnRK2.2/2.3/2.6 (subgroup III), are specifically activated by ABA and play a central role in the ABA pathway [9]. PP2Cs seem to regulate SnRK2s through physical obstruction and through direct dephosphorylation of the conserved S175 residue in the T-loop [9, 10]. In the presence of ABA the PYR/PYL/RCAR family of ABA receptors sequester PP2Cs, resulting in the activation of SnRK2s and its downstream transcription factors and target genes[9, 10]. Genetic screens have revealed extensive interactions between sugar and ABA-response pathways, but the underlying components have remained elusive [11]. We postulate that this interaction originates in the crosstalk between the SnRK1 and SnRK2 pathways and we propose a combination of transient assays, biochemistry, proteomics, and gain- and loss-of-function analyses, to test this.
|
