Dissection of general and specific regulatory mechanism of sulfur metabolism in Arabidopsis thaliana

生长和翻译的减少是植物对各种胁迫的一种普遍反应，作为一种权衡，以释放能量用于胁迫反应。该项目解决了植物研究的一个基本问题：蛋白质翻译和分生组织活动在矿物质营养缺乏下是如何调节的？这些过程的协调是至关重要的驯化反应，如在地上部-根比的变化。在前面的研究中，我们研究了拟南芥的硫酸盐同化途径及其特定的调控机制。我们专注于半胱氨酸，因为它是协调硫与碳和氮同化的中心代谢物。对导致半胱氨酸的途径的硫或碳/氮分支的通量受限的突变体的比较揭示了激酶GCN 2（一般对照非去阻遏2）和TOR（雷帕霉素的靶标）的特异性传感机制。我们发现，这两个独立的控制翻译和生长的芽和根，植物TOR传感硫的可用性通过下调葡萄糖-TOR信号转导。TOR调控网络包括诱导自噬和下调翻译和分生组织活性。这些发现提供了基础，以解开不同的营养线索对协调变化的植物生长调节的整合。本研究的第一部分，我们将解决TOR调节的特异性后，限制不同的矿物质营养素。这将使我们能够从控制硫缺乏特异性反应的信号中剖析TOR编排的诱导对营养限制的一般反应的信号。进一步的重点将放在硫缺乏诱导的TOR调节的上游信号转导机制上。在研究的第二部分，我们将揭示TOR如何调节下游过程以实现适应反应。在这方面，TOR的主要目标是控制蛋白质组的可塑性，通过自噬和泛素/蛋白酶体系统进行营养物质的再循环，以及响应硫可用性的细胞周期。总之，这些方法将解释TOR支配的过程，这些过程对于理解硫调节网络是不可或缺的，硫调节网络可以被视为初级营养物质代谢的角色模型。

Decrease of growth and translation is a general response of plants to diverse stresses as a trade-off to release energy for stress responses. This project addresses a fundamental question of plant research: How is protein translation and meristem activity regulated under mineral-nutrient deficiency? The coordination of these processes is crucial for acclimation responses such as shifts in shoot-to-root-ratio. In the previous proposal we investigated the sulfate assimilation pathway and its specific regulatory mechanisms in Arabidopsis thaliana. We focused on cysteine since it is the central metabolite that coordinates the assimilation of sulfur with that of carbon and nitrogen. The comparison of mutants that are either limited in flux of the sulfur or carbon/nitrogen branch of the pathway leading to cysteine revealed specific sensing mechanisms by the kinases GCN2 (general control non-derepressible 2) and TOR (target of rapamycin). We showed that both contribute independently to control of translation and growth of shoot and root and that plant TOR senses sulfur availability in leaves via down-regulation of glucose-TOR signaling. The TOR regulated network included induction of autophagy and down-regulation of translation and meristematic activity. These findings provide the basis to unravel the integration of different nutritional cues towards coordinated changes in plant growth regulation. The first part of this study we will address the specificity of TOR regulation upon limitation of diverse mineral nutrients. This will allow us to dissect the signals for the induction of the general response to nutrient limitation orchestrated by TOR from the signals controlling the sulfur deficiency specific response. Further emphasis will be given on the upstream signal transduction machinery for the sulfur deficiency-induced regulation of TOR. In the second part of the study we will unravel how TOR regulates downstream processes to achieve acclimation responses. Prime targets of TOR in this respect are the control of the plasticity of the proteome, the recycling of nutrients by autophagy and the ubiquitin/proteasome system, and the cell cycle in response to sulfur availability. Together, these approaches will explain TOR governed processes that are integral for the understanding of the sulfur regulatory network that can be seen as a role model for primary nutrient metabolism.