Involvement of the SnRK1 subunit KIN10 in sucrose-induced hypocotyl elongation

Noriane Simon, Ellie Sawkins, Antony Dodd*

*Corresponding author for this work

Research output: Contribution to journalArticle (Academic Journal)peer-review

6 Citations (Scopus)
190 Downloads (Pure)


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.
Original languageEnglish
Article numbere1457913
Number of pages3
JournalPlant Signaling and Behavior
Early online date27 Mar 2018
Publication statusE-pub ahead of print - 27 Mar 2018


  • Arabidopsis
  • development
  • metabolism
  • signal transduction

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