RETINOBLASTOMA-RELATED PROTEIN controls the transition to autotrophic plant development
RETINOBLASTOMA-RELATED PROTEIN controls the transition to autotrophic plant development
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DOI：
10.1242/dev.060830
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发表时间：
2011-07-15
期刊：
影响因子：
4.6
通讯作者：
Gruissem, Wilhelm
中科院分区：
文献类型：
--
作者：
Gutzat, Ruben;Borghi, Lorenzo;Gruissem, Wilhelm
在植物发育过程中，萌发的异养胚胎转入自养生长发育过程中，成苗是一个关键阶段。胚胎发育的正调控因子需要关闭，而细胞周期机制被激活，以允许细胞周期进入和器官原基启动。然而，目前还不清楚在这一转变过程中，负责细胞分裂开始、代谢变化和细胞分化的分子机制是如何协调的。在这里，我们证明了动物肿瘤抑制因子视网膜母细胞瘤(PRB)的拟南芥视网膜母细胞瘤相关蛋白(RBR)同源基因不仅控制细胞周期相关基因的表达，而且通过增加组蛋白H3K27的三甲基化来持续关闭晚期胚胎基因。RBR功能降低的幼苗萌发后发育停滞，低浓度蔗糖刺激诱导晚期胚胎基因转录，导致异位细胞分裂。我们的结果提出了一个模型，在该模型中，RBR通过负调控细胞周期和抑制胚胎基因来对抗蔗糖。因此，RBR是胚胎异养生长向自养生长转变的正向调节因子。这使RBR成为新陈代谢和发育决策的新整合者。
Seedling establishment is a crucial phase during plant development when the germinating heterotrophic embryo switches to autotrophic growth and development. Positive regulators of embryonic development need to be turned off, while the cell cycle machinery is activated to allow cell cycle entry and organ primordia initiation. However, it is not yet understood how the molecular mechanisms responsible for the onset of cell division, metabolism changes and cell differentiation are coordinated during this transition. Here, we demonstrate that the Arabidopsis thaliana RETINOBLASTOMA-RELATED protein (RBR) ortholog of the animal tumor suppressor retinoblastoma (pRB) not only controls the expression of cell cycle-related genes, but is also required for persistent shut-down of late embryonic genes by increasing their histone H3K27 trimethylation. Seedlings with reduced RBR function arrest development after germination, and stimulation with low amounts of sucrose induces transcription of late embryonic genes and causes ectopic cell division. Our results suggest a model in which RBR acts antagonistically to sucrose by negatively regulating the cell cycle and repressing embryonic genes. Thus, RBR is a positive regulator of the developmental switch from embryonic heterotrophic growth to autotrophic growth. This establishes RBR as a new integrator of metabolic and developmental decisions.