Seed development passes through developmental phases such as cell division, differentiation and maturation: each have specific metabolic demands. The ubiquitous sucrose non-fermenting-like kinase (SnRK1) coordinates and adjusts physiological and metabolic demands with growth. In protoplast assays sucrose deprivation and hormone supplementation, such as with auxin and abscisic acid (ABA), stimulate SnRK1-promoter activity. This indicates regulation by nutrients: hormonal crosstalk under conditions of nutrient demand and cell proliferation. SnRK1-repressed pea (Pisum sativum) embryos show lower cytokinin levels and deregulation of cotyledonary establishment and growth, together with downregulated gene expression related to cell proliferation, meristem maintenance and differentiation, leaf formation, and polarity. This suggests that at early stages of seed development SnRK1 regulates coordinated cotyledon emergence and growth via cytokinin-mediated auxin transport and/or distribution. Decreased ABA levels and reduced gene expression, involved in ABA-mediated seed maturation and response to sugars, indicate that SnRK1 is required for ABA synthesis and/or signal transduction at an early stage. Metabolic profiling of SnRK1-repressed embryos revealed lower levels of most organic and amino acids. In contrast, levels of sugars and glycolytic intermediates were higher or unchanged, indicating decreased carbon partitioning into subsequent pathways such as the tricarbonic acid cycle and amino acid biosynthesis. It is hypothesized that SnRK1 mediates the responses to sugar signals required for early cotyledon establishment and patterning. As a result, later maturation and storage activity are strongly impaired. Changes observed in SnRK1-repressed pea seeds provide a framework for how SnRK1 communicates nutrient and hormonal signals from auxins, cytokinins and ABA to control metabolism and development.