Unraveling the Link between Carbohydrate Transport and Phosphate Use: Can We Improve Carbon Partitioning and Reduce Nutrient Use?

在提高作物产量的同时减少农业对环境的影响是突出的挑战。磷酸盐是一种必需的营养素，但也是农业径流和水污染的主要成分。 增加光合作用和糖从叶子到生长器官的运输被假设为增加整体生长，但新的证据认为，这造成了光合作用碳（光合作用产生的糖）和可用磷酸盐比例的不平衡，并导致发育迟缓。 更多的磷酸盐恢复生长，但也有助于更多的径流。 这意味着，除非碳和磷酸盐之间的相互作用被理解和解偶联，否则在提高光合作用和生长的同时减少磷酸盐需求的努力可能会受到威胁。 这项建议旨在区分两种可能性。 1)碳/磷酸盐相互作用主要是一种生化限制：生长组织中的碳越多，就需要更多含磷酸盐的代谢物。 2)植物测量碳/磷酸盐平衡，过量的碳被认为是磷酸盐缺乏，即使不存在。 这些将通过生理、遗传和代谢实验进行测试，以了解碳运输和磷酸盐需求之间的联系是否可以分开。这项工作将揭示可用于提高生产力同时减少肥料需求的策略。除了学生在研究实验室的传统培训，更广泛的本科生参与将通过将该项目的某些方面纳入上层植物生理学实验室本科课程实现。每年大约有30名学生参加该课程，他们将学习遗传学，分子生物学和生物信息学的原理。这不仅将在积极的学习环境中提供实践生物技术经验，但也将作为一个机会，探讨转基因生物'转基因'辩论与一组大学生谁否则可能不太可能参与这一重要的社会问题。增强蔗糖运输从源叶到库器官应提高作物产量，提供更多的资源，为生长，同时减轻产品抑制关于光合作用。在韧皮部中过度表达蔗糖转运蛋白（SUTs）增强了运输，但由于感知到的磷（P）缺乏而导致生长发育迟缓：P饥饿基因上调，并且该效应被P补充逆转。磷是一种不可再生的基本元素，也是农业径流的一个组成部分，因此在保持产量的同时减少磷的需求也是一个突出的挑战。一种可能性是，更多的蔗糖通过在代谢中间产物中螯合太多的P而导致发育迟缓。另一种可能性是碳（C）和磷之间的信号传导引发了磷限制的准备。这些将通过实验进行测试，包括1）用亚磷酸盐作为磷酸盐类似物生长以分离信号传导和生物化学效应; 2）反向和正向遗传学以鉴定调节C：P相互作用的基因; 3）转录组学以捕获Suc诱导的P限制期间的基因表达重新优先化; 4）代谢分析以捕获Suc诱导的P限制期间的代谢组重塑;以及5）通过功能线的获得和损失的生理学实验来了解C：P连接是否可以解偶联。

Increasing crop productivity while reducing environmental impacts of agriculture are prominent challenges. Phosphate is an essential nutrient, but is also a major component of agricultural runoff and water pollution. Increased photosynthesis and transport of sugars from leaves to growing organs was hypothesized to increase overall growth, but new evidence argues that this creates an imbalance in the ratio of photoassimilated carbon (the sugars produced by photosynthesis) and available phosphate, and causes stunting. More phosphate restores growth, but also contributes to more runoff. The implication is that efforts to improve photosynthesis and growth while simultaneously reducing phosphate requirements may be imperiled unless the interaction between carbon and phosphate is understood and uncoupled. This proposal aims to differentiate between two possibilities. 1) The carbon/phosphate interaction is predominantly a biochemical limitation: more carbon in growing tissues triggers a need for more phosphate-containing metabolites. 2) The plant measures the carbon/phosphate balance, and excessive carbon is recognized as a phosphate deficiency even though none exists. These will be tested through physiological, genetic, and metabolic experiments to learn if the links between carbon transport and phosphate needs can be uncoupled. This work will reveal strategies that can be used to increase productivity while reducing fertilizer needs. In addition to traditional training of students in the research laboratory, broader undergraduate participation will be achieved by incorporating some aspects of the project into the upper level Plant Physiology laboratory undergraduate course. The approximately 30 students who take the course each year will learn principles of genetics, molecular biology, and bioinformatics. This will not only give hands-on biotechnology experience in an active-learning environment, but also will be used as an opportunity to explore the Genetically Modified Organisms 'GMO' debate with a group of undergraduates who might otherwise be unlikely to engage with this important societal issue.Enhanced sucrose transport from source leaves to sink organs should improve crop yields by providing more resources for growth while relieving product inhibition on photosynthesis. Over-expressing sucrose transporters (SUTs) in the phloem enhances transport but causes stunted growth originating from a perceived phosphorus (P) deficiency: P-starvation genes are up-regulated and the effect is reversed by P supplementation. P is a non-renewable essential element and a component of agricultural runoff, such that reducing P requirements while maintaining yields are also prominent challenges. One possibility is that more sucrose causes stunting by sequestering too much P in metabolic intermediates. Another possibility is that signaling between carbon (C) and P provokes preparation for P-limitation. These will be tested through experiments that include 1) growth with phosphite as a phosphate analog to separate signaling and biochemical effects; 2) reverse and forward genetics to identify genes that modulate C:P interaction; 3) transcriptomics to capture gene-expression reprioritization during Suc-induced P-limitations; 4) metabolic analyses to capture metabolome remodeling during Suc-induced P-limitations; and 5) physiological experiments with gain and loss of function lines to learn if C:P links can be uncoupled.