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

在提高作物生产力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物质，但也是农业径流和水污染的主要组成部分。据推测，增加的光合作用和糖从叶片到生长器官的运输可以促进整体生长，但新的证据表明，这造成了光同化碳（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。更多的磷酸盐可以恢复生长，但也会导致更多的径流。这意味着，除非碳和磷酸盐之间的相互作用被理解和解耦，否则提高光合作用和生长同时减少磷酸盐需求的努力可能会受到危害。这个提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：生长组织中更多的碳会触发对更多含磷酸盐代谢物的需求。2)植物测量碳/磷酸盐平衡，即使不存在，过量的碳也被认为是磷酸盐缺乏。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解耦。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。除了传统的学生在研究实验室的训练外，通过将项目的某些方面纳入更高层次的植物生理学实验室本科课程，可以实现更广泛的本科生参与。每年大约有30名学生参加这门课程，他们将学习遗传学、分子生物学和生物信息学的原理。这不仅能让学生在主动学习的环境中亲身体验生物技术，而且还将作为一个机会，与一群本科生探讨转基因生物（GMO）的辩论，否则他们可能不太可能参与这一重要的社会问题。增强蔗糖从源叶到汇器官的转运，为作物提供更多的生长资源，同时减轻产物对光合作用的抑制，从而提高作物产量。韧皮部中蔗糖转运蛋白（SUTs）的过度表达促进了运输，但由于磷(P)缺乏而导致生长迟缓：缺磷基因被上调，而补磷可以逆转这一效应。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对磷的需求也是一个突出的挑战。一种可能性是，过多的蔗糖通过在代谢中间体中吸收过多的磷而导致发育迟缓。另一种可能性是碳(C)和磷之间的信号引发了限制磷的准备。这些将通过以下实验进行测试：1)以亚磷酸盐作为磷酸盐类似物进行生长，以分离信号和生化效应；2)反向遗传学和正向遗传学鉴定调节C:P相互作用的基因；3)转录组学捕获在suc诱导的p限制期间基因表达的重优先级；4)代谢分析，以捕捉在suc诱导的p限制期间代谢组重塑；5)生理实验的增益和损失的功能线，以了解是否可以解耦C:P链接。

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.