Ureide metabolism in response to abiotic stress in plants

在植物中，尿素代谢通常与固氮的“热带”豆类（如大豆和普通豆）有关，因为从根瘤通过木质部运输的氮中，高达95%是以尿囊素和尿囊酸盐两种尿素化合物的形式存在的。最近，尿囊素和尿囊酸盐的积累与其他物种对非生物胁迫的反应有关，包括水稻和拟南芥。尿囊素水平升高可以保护机体免受多种非生物应激，并减少应激诱导的活性氧。我们的目标是通过研究尿素合成和分解代谢的调节，确定这种反应的细胞基础，并确定所涉及的信号通路，来了解尿素代谢和非生物应激是如何联系在一起的。

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.