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Cytosolic invertase 1 (CINV1), which converts sucrose into glucose and fructose is a key entry point of carbon into cellar metabolism and Hexokinase 1 (HXK1) functions as a pivotal sensor for glucose. Further, it is well established that sugar signaling can regulate plant gene expression, for example, the Production of Anthocyanin Pigment 1 (PAP1) / MYB75 transcription factor is specifically induced by sucrose accumulation. Exogenous sugars are also thought to trigger the juvenile-to-adult phase transition via a miR156A/SQUAMOSA PROMOTER BINDING PROTEIN-LIKE (SPL) module. However, the endogenous factors that regulate this process have remained undetermined. Here we show that sucrose induced expression of the PAP1 transcription factor increases CINV1 activity by direct binding to CINV1 promoter. Further, we identify a glucose feed-forward loop (Sucrose-CINV1-Glucose-HXK1-miR156-SPL9-PAP1-CINV1-Glucose) that controls CINV1 activity to convert sucrose into glucose signaling to dynamically control the juvenile-to-adult phase transition. Moreover, PAP1 directly binds to the SPL9 promoter, activating SPL9 expression, triggering sucrose signaling that mediates the juvenile-to-adult phase transition. Therefore, a glucose signaling feed-forward loop and a sucrose signaling pathway synergistically regulate the Arabidopsis juvenile-to-adult phase transition. Collectively, we identify a molecular link between the major photosynthate sucrose, the entry point of carbon into cellar metabolism and a key developmental process, the juvenile-to-adult phase transition.

De-etiolation is indispensable for seedling survival and development. However, how sugars regulate de-etiolation and how sugars induce ethylene (ET) for seedlings to grow out of soil remain elusive. Here, we reveal how a sucrose (Suc) feedback loop promotes de-etiolation by inducing ET biosynthesis. Under darkness, Suc in germinating seeds preferentially induces 1-amino-cyclopropane-1-carboxylate synthase (ACS7; encoding a key ET biosynthesis enzyme) and associated ET biosynthesis, thereby activating ET core component ETHYLENE-INSENSITIVE3 (EIN3). Activated EIN3 directly inhibits the function of Suc transporter 2 (SUC2; a major Suc transporter) to block Suc export from cotyledons and thereby elevate Suc accumulation of cotyledons to induce ET. Under light, ET-activated EIN3 directly inhibits the function of phytochrome A (phyA; a de-etiolation inhibitor) to promote de-etiolation. We therefore propose that under darkness, the Suc feedback loop (Suc-ACS7-EIN3-|SUC2-Suc) promotes Suc accumulation in cotyledons to guarantee ET biosynthesis, facilitate de-etiolation, and enable seedlings to grow out of soil.