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The Energy-Signaling Hub SnRK1 Is Important for Sucrose-Induced Hypocotyl Elongation

Research output: Contribution to journalArticle

  • Noriane Simon
  • Jelena Kusakina
  • Angela Fernandez-Lopez
  • Anupama Chembath
  • Fiona Belbin
  • Antony Dodd
Original languageEnglish
Pages (from-to)1299-1310
Number of pages12
JournalPlant Physiology
Early online date7 Nov 2017
DateAccepted/In press - 5 Nov 2017
DateE-pub ahead of print - 7 Nov 2017
DatePublished (current) - 6 Feb 2018


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 signalling pathways that integrate environmental information to regulate seedling development. The hypocotyls of 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 sucrose. We focused upon the role of SnRK1, which is a sugar-signalling hub that regulates metabolism and transcription in response to cellular energy status. We also investigated the role of TPS1, an enzyme that synthesizes the signalling sugar trehalose-6-phosphate (Tre6P) that is proposed to regulate SnRK1 activity. Under light/dark cycles, we found that sucrose-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 sucrose-induced hypocotyl elongation depends on the day length and light intensity. We identified roles for auxin and gibberellin signalling in sucrose-induced hypocotyl elongation under short photoperiods. We found that sucrose-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 sucrose-induced hypocotyl elongation in light/dark cycles.

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