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

提高作物生产力，同时减少农业对环境的影响是突出的挑战。磷酸盐是一种基本的营养物质，但也是农业径流和水污染的主要成分。光合作用的增加和糖从叶片到生长器官的运输被认为是为了促进整体生长，但新的证据表明，这会造成光合作用产生的碳同化和有效磷的比例失衡，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，除非了解碳和磷之间的相互作用并解除耦合，否则在降低磷需求的同时改善光合作用和生长的努力可能会受到威胁。这项提议旨在区分两种可能性。1)碳/磷的相互作用主要是一种生化限制：生长组织中碳的增加引发了对更多含磷代谢物的需求。2)植物测量碳/磷平衡，过量的碳被认为是一种磷缺乏，即使不存在。这些将通过生理、遗传和新陈代谢实验进行测试，以了解碳运输和磷酸盐需求之间的联系是否可以分离。这项工作将揭示在减少化肥需求的同时提高生产率的策略。除了在研究实验室对学生进行传统的培训外，通过将该项目的某些方面纳入高级植物生理学实验室本科课程，将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，学习遗传学、分子生物学和生物信息学的原理。这不仅将提供积极学习环境中的实践生物技术经验，还将被用作与一群本科生探讨转基因生物的辩论的机会，否则他们可能不太可能参与这一重要的社会问题。加强蔗糖从源叶到汇器官的运输应该会通过提供更多的生长资源来提高作物产量，同时缓解产品对光合作用的抑制。在韧皮部过表达的蔗糖转运体(SUT)促进了运输，但由于感知到的磷(P)缺乏而导致生长受阻：磷饥饿基因上调，这种作用被磷补充逆转。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，更多的蔗糖通过将过多的磷隔离在代谢中间产物中而导致发育迟缓。另一种可能性是碳(C)和磷之间的信号传递引发了对磷限制的准备。这些实验包括：1)用亚磷酸盐作为磷酸盐类似物生长，以分离信号和生化效应；2)反向和正向遗传学，以确定调节C：P相互作用的基因；3)转录组学，以捕捉Suc诱导的P限制期间基因表达的重新优先顺序；4)代谢分析，以捕捉Suc诱导的P限制期间的代谢组重构；以及5)获得和失去功能线的生理实验，以了解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.