Meng Lai-Sheng, Li Ying-Qiu, Liu Meng-Qian, Jiang Ji-Hong
The Key Laboratory of Biotechnology for Medicinal Plant of Jiangsu Province, School of Life Science, Jiangsu Normal UniversityXuzhou, China; Centre for Transformational Biotechnology of Medicinal and Food Plants, Jiangsu Normal University - Edinburgh UniversityXuzhou, China.
Front Plant Sci. 2016 Nov 22;7:1728. doi: 10.3389/fpls.2016.01728. eCollection 2016.
Anthocyanin accumulation specifically depends on sucrose (Suc) signaling/levels. However, the gene cascades specifically involved in the Suc signaling/level-mediated anthocyanin biosynthetic pathway are still unknown. (), a transcription coactivator, is involved in the regulation of leaf shape and drought tolerance. Recently, an gene cascade has been reported to regulate the light signaling-mediated anthocyanin accumulation. Target gene analysis indicates that is associated with the () promoter, a mitogen-activated protein kinase kinase kinase, for inducing anthocyanin accumulation. Indeed, loss-of-function mutants of showed significantly increased anthocyanin accumulation. mutation can also suppress the decrease in anthocyanin accumulation. Further analysis indicates that the mutations of and disrupt the normal Suc levels because of the changes of invertase activity in mutants of or , which in turn induces the alterations of anthocyanin accumulation in mutants of or via unknown regulatory mechanisms.
花青素的积累特别依赖于蔗糖(Suc)信号/水平。然而,蔗糖信号/水平介导的花青素生物合成途径中具体涉及的基因级联反应仍然未知。(),一种转录共激活因子,参与叶片形状和耐旱性的调控。最近,有报道称一种基因级联反应可调节光信号介导的花青素积累。靶基因分析表明,()与()启动子相关,()是一种丝裂原活化蛋白激酶激酶激酶,可诱导花青素积累。事实上,()功能缺失突变体的花青素积累显著增加。()突变也可抑制()花青素积累的减少。进一步分析表明,()和()的突变会因()或()突变体中转化酶活性的变化而破坏正常的蔗糖水平,进而通过未知调控机制诱导()或()突变体中花青素积累的改变。