Abscisic acid deficiency of developing pea embryos achieved by immunomodulation attenuates developmental phase...

The transition of pea embryos from pre-storage to maturation is partially controlled by abscisic acid (ABA). Immunomodulation in pea embryos specifically reduces free ABA levels during transition stages. Such seeds are, therefore, suitable models for studying ABA deficiency by global transcript and metabolite analysis. Compared with the wild type, anti-ABA seeds are smaller, contain fewer globulins and show lower dry matter accumulation and delayed differentiation. Free sugars are decreased, indicating lower uptake and/or elevated mobilisation. Lower levels of trans-zeatins suggest that ABA reduction influences rates of cytokinin synthesis and/or its level of accumulation. Abscisic acid deficiency leads to a general downregulation of gene expression related to transcription and translation. At the transcriptional level, anti-ABA embryos reveal a wide-range repression of carbohydrate oxidation, downregulated sucrose mobilisation, glycolysis and the tricarboxylic acid cycle/Krebs cycle (TCA cycle). Genes related to starch, amino acid and storage protein biosynthesis are downregulated, indicating a general decrease in metabolic fluxes. We conclude that during embryo differentiation ABA triggers broad upregulation of gene activity and genetic reprogramming, involving regulated protein degradation via the ubiquitin/proteasome system. Abscisic acid deficiency affects gene expression associated with transport processes and stimulation of membrane energisation. Our study identified mediators and downstream signalling elements of ABA during embryo differentiation, such as the transcription factor FUSCA3, SnRK1 kinase and Ca(2+) signalling processes. This suggests that ABA interacts with SnRK1 complexes, thus connecting SnRK1, sugar and stress signalling with ABA. Certain protein kinases/phosphatases known to negatively respond to ABA are upregulated in the modulated line, whilst those which respond positively are downregulated, pointing to a highly coordinated response of the gene network to ABA levels.