Ureide metabolism in response to abiotic stress in plants

在植物中，酰脲代谢通常与固氮的“热带”豆类如大豆和菜豆有关，因为高达95%的从根瘤通过木质部运输的氮以两种酰脲化合物尿囊素和尿囊酸的形式存在。 最近，尿囊素和尿囊酸的积累与其他物种（包括水稻和拟南芥）对非生物胁迫的反应有关。 高水平的尿囊素赋予保护免受广泛的非生物胁迫，并减少胁迫诱导的活性氧。我们的目标是了解如何酰脲代谢和非生物胁迫是通过检查酰脲合成和catalysts的调节，确定这种反应的细胞基础，并确定参与的信号通路。 在响应非生物胁迫，包括干旱，强光，或处理与重金属如镉，酰脲尿囊素积累在植物组织中，伴随着上游酶如尿酸氧化酶的基因编码的上调，和尿囊素酶基因的表达下调和降低尿囊素酶活性。尿囊素本身对非生物胁迫具有一定程度的抗性或耐受性，这表明尿囊素积累在响应胁迫中具有特定的生理作用。这些治疗的共同点是它们都有助于氧化应激和植物细胞中活性氧的产生。 我们目前的模型提出，尿囊素通过激活抗氧化酶，清除活性氧，如过氧化氢和超氧化物，减轻氧化应激。 这降低了细胞暴露于的氧化应激，并且当将野生型对照与缺乏尿囊素的突变体进行比较时，或者当将已经用尿囊素处理的植物与未处理的植物进行比较时，允许植物更好地耐受这些条件。 我们实验室和其他人迄今收集的数据表明，这可能涉及ABA依赖性和ABA非依赖性信号通路。 我们计划调查这两者之间的联系。 在理解这一机制，我们试图回答的问题，包括，什么是氧化应激和酰脲积累在细胞水平之间的空间和时间关系？ 尿囊素介导的抗氧化途径上调涉及哪些途径和机制？ 在理想条件和胁迫条件下，尿囊素介导的非生物胁迫耐受性的代谢或适应性代价是什么？在经济作物物种中是否可以操纵这一途径以提高胁迫耐受性？我们的目标是有助于更好地理解这一过程，最终目的是提高植物的抗逆性。

In plants, ureide metabolism is often associated with nitrogen-fixing “tropical” legumes such as soybean and common bean because up to 95% of nitrogen transported from root nodules through the xylem is in the form of two ureide compounds, allantoin and allantoate. Recently, accumulation of allantoin and allantoate has been associated with response to abiotic stresses in other species, including rice and Arabidopsis. Elevated levels of allantoin confers protection from a wide range of abiotic stresses, and decreases stress-induced reactive oxygen species. Our goal is to understand how ureide metabolism and abiotic stress are linked by examining the regulation of ureide synthesis and catabolism, determining the cellular basis of this response, and identifying the signaling pathway(s) involved. In response to abiotic stressors including drought, high light, or treatment with heavy metal such as cadmium, the ureide allantoin accumulates in plant tissues accompanied by up-regulation of genes coding for upstream enzymes such as urate oxidase, and down-regulation of allantoinase gene expression and decreased allantoinase enzyme activity. Allantoin itself confers some degree of resistance or tolerance to abiotic stressors, pointing to a specific physiological role for allantoin accumulation in response to stress. What these treatments have in common is that they all contribute to oxidative stress and generation of reactive oxygen species in plant cells. Our current model proposes that allantoin alleviates oxidative stress through activation of antioxidant enzymes that remove reactive oxygen species such as hydrogen peroxide and superoxide. This decreases the oxidative stress cells are exposed to and allow the plants to tolerate these conditions better when comparing wild-type controls to mutants lacking allantoinse, or when comparing plants that have been treated with allantoin to untreated plants. Data gathered to date by our lab and others suggest that this may involve both ABA-dependent and ABA-independent signaling pathways. We plan to investigate the connection. In understanding this mechanism we seek to answer questions that include, What is the spatial and temporal relationship between oxidative stress and ureide accumulation at the cellular level? What pathways and mechanisms are involved in allantoin-mediated upregulation of antioxidant pathways? What is the metabolic or fitness cost of allantoin-mediated abiotic stress tolerance under ideal and stress conditions? Can this pathway be manipulated in economically crop species to improve stress tolerance? The goal is to contribute to a better understanding of this process, with an ultimate aim of improving plant stress tolerance in plants.