Emerging seedlings respond to environmental conditions such as light and temperature to optimize their establishment. Seedlings grow initially through elongation of the hypocotyl, which is regulated by signaling pathways that integrate environmental information to regulate seedling development. The hypocotyls of Arabidopsis (Arabidopsis thaliana) also elongate in response to sucrose. Here, we investigated the role of cellular sugar-sensing mechanisms in the elongation of hypocotyls in response to Suc. We focused upon the role of SnRK1, which is a sugar-signaling hub that regulates metabolism and transcription in response to cellular energy status. We also investigated the role of TPS1, which synthesizes the signaling sugar trehalose-6-P that is proposed to regulate SnRK1 activity. Under light/dark cycles, we found that Suc-induced hypocotyl elongation did not occur in tps1 mutants and overexpressors of KIN10 (AKIN10/SnRK1.1), a catalytic subunit of SnRK1. We demonstrate that the magnitude of Suc-induced hypocotyl elongation depends on the day length and light intensity. We identified roles for auxin and gibberellin signaling in Suc-induced hypocotyl elongation under short photoperiods. We found that Suc-induced hypocotyl elongation under light/dark cycles does not involve another proposed sugar sensor, HEXOKINASE1, or the circadian oscillator. Our study identifies novel roles for KIN10 and TPS1 in mediating a signal that underlies Suc-induced hypocotyl elongation in light/dark cycles.

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A mechanism participating in energy sensing and signalling in plants involves the regulation of sucrose non-fermenting1 (Snf1)-related protein kinase 1 (SnRK1) activity in response to sugar availability. SnRK1 is thought to regulate the activity of both metabolic enzymes and transcription factors in response to changes in energy availability, with trehalose-6-phospate functioning as a signalling sugar that suppresses SnRK1 activity under sugar-replete conditions. Sucrose supplementation increases the elongation of hypocotyls of developing Arabidopsis seedlings, and this response to sucrose involves both the SnRK1 subunit KIN10 and also TREHALOSE-6-PHOSPHATE SYNTHASE1 (TPS1). Here, we measured sucrose-induced hypocotyl elongation in two insertional mutants of KIN10 (akin10 and akin10-2). Under short photoperiods, sucrose supplementation caused great proportional hypocotyl elongation in these KIN10 mutants compared with the wild type, and these mutants had shorter hypocotyls than the wild type in the absence of sucrose supplementation. One interpretation is that SnRK1 activity might suppress hypocotyl elongation in the presence of sucrose, because KIN10 overexpression inhibits sucrose-induced hypocotyl elongation and akin10 mutants enhance sucrose-induced hypocotyl elongation.

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