Plant Biology and Crop Science, Rothamsted Research, Harpenden, Hertfordshire AL5 2JQ, United Kingdom.
Plant Physiol. 2013 Jul;162(3):1720-32. doi: 10.1104/pp.113.220657. Epub 2013 Jun 4.
Trehalose 6-P (T6P) is a sugar signal in plants that inhibits SNF1-related protein kinase, SnRK1, thereby altering gene expression and promoting growth processes. This provides a model for the regulation of growth by sugar. However, it is not known how this model operates under sink-limited conditions when tissue sugar content is uncoupled from growth. To test the physiological importance of this model, T6P, SnRK1 activities, sugars, gene expression, and growth were measured in Arabidopsis (Arabidopsis thaliana) seedlings after transfer to cold or zero nitrogen compared with sugar feeding under optimal conditions. Maximum in vitro activities of SnRK1 changed little, but T6P accumulated up to 55-fold, correlating with tissue Suc content in all treatments. SnRK1-induced and -repressed marker gene expression strongly related to T6P above and below a threshold of 0.3 to 0.5 nmol T6P g(-1) fresh weight close to the dissociation constant (4 µm) of the T6P/ SnRK1 complex. This occurred irrespective of the growth response to Suc. This implies that T6P is not a growth signal per se, but through SnRK1, T6P primes gene expression for growth in response to Suc accumulation under sink-limited conditions. To test this hypothesis, plants with genetically decreased T6P content and SnRK1 overexpression were transferred from cold to warm to analyze the role of T6P/SnRK1 in relief of growth restriction. Compared with the wild type, these plants were impaired in immediate growth recovery. It is concluded that the T6P/SnRK1 signaling pathway responds to Suc induced by sink restriction that enables growth recovery following relief of limitations such as low temperature.
海藻糖-6-磷酸(T6P)是植物中的一种糖信号,它可抑制 SNF1 相关蛋白激酶(SnRK1),从而改变基因表达并促进生长过程。这为糖对生长的调控提供了模型。然而,当组织糖含量与生长解偶联时,这种模型在受限于汇的条件下是如何运作的还不得而知。为了检验该模型的生理重要性,在与最优条件下糖喂养相比,将拟南芥(Arabidopsis thaliana)幼苗转移到冷或零氮条件下后,测定了 T6P、SnRK1 活性、糖、基因表达和生长情况。SnRK1 的最大体外活性变化不大,但 T6P 积累了多达 55 倍,与所有处理中的组织蔗糖含量相关。SnRK1 诱导和抑制的标记基因表达与 T6P 强烈相关,T6P 高于或低于 0.3 到 0.5 nmol T6P g(-1) 鲜重的阈值,接近 T6P/SnRK1 复合物的离解常数(4 µm)。这与对 Suc 的生长反应无关。这意味着 T6P 本身不是生长信号,而是通过 SnRK1,T6P 在汇限制下响应 Suc 积累,为生长做好准备。为了验证这一假设,从冷到热将 T6P 含量降低和 SnRK1 过表达的植物转移,以分析 T6P/SnRK1 在缓解生长限制中的作用。与野生型相比,这些植物在即时生长恢复方面受损。结论是,T6P/SnRK1 信号通路对由汇限制诱导的 Suc 做出反应,使生长在解除低温等限制后得以恢复。