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

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 (<i>akin10</i> and <i>akin10</i>-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 <i>akin10</i> mutants enhance sucrose-induced hypocotyl elongation.

植物体内参与能量感知与信号转导的一类机制，会响应糖类可利用性，对蔗糖非发酵1（Snf1）相关蛋白激酶1（SnRK1）的活性进行调控。现有研究表明，SnRK1可响应能量可利用性的变化，同时调控代谢酶与转录因子的活性；其中海藻糖-6-磷酸（trehalose-6-phosphate）作为信号糖类，在糖充足条件下可抑制SnRK1的活性。外源添加蔗糖可促进发育中拟南芥幼苗下胚轴的伸长，这一蔗糖响应过程同时依赖SnRK1亚基KIN10与海藻糖-6-磷酸合酶1（TPS1）。本研究针对KIN10的两个插入突变体（akin10与akin10-2），检测了蔗糖诱导的下胚轴伸长现象。在短日照条件下，相较于野生型，这两种KIN10突变体经蔗糖补充处理后，下胚轴的相对伸长量更为显著；且在未添加蔗糖的培养条件下，突变体的下胚轴长度短于野生型。一种合理的解释是：SnRK1活性可能在蔗糖存在时抑制下胚轴伸长——这一推论得到以下实验结果的支撑：过表达KIN10会抑制蔗糖诱导的下胚轴伸长，而akin10突变体则会增强该诱导伸长效应。