Joint NSF/ERA-CAPS: Al-UCIDATE - Towards A Molecular Understanding of Aluminum Genotoxicity for Crop Improvement

PI：Paul Larsen(加州大学河滨分校)ERA-CAPS合作者：Liven DeVeylder(比利时根特大学)、Arp Schnittger(德国汉堡大学)和Iwan a Szarejko(波兰塞伦西亚大学卡托维兹分校)铝毒性是全球农作物生产的一个重要限制因素，世界上50%以上的可耕地都存在铝中毒。铝毒害最明显的症状和重要后果是对酸性土壤的根生长抑制。一个突出的例子是大麦，它是包括欧洲和北美在内的温带地区最重要的作物之一。大麦对铝毒非常敏感，在酸性土壤中生长造成的产量损失高达30%。以前一直认为，铝的毒性是一个棘手的问题，因为它明显的复杂性。本项目的目标是确定在长期铝暴露后抑制拟南芥和大麦根生长的生化机制。人们期望，对这一新过程的包容性理解将使农业作物能够在铝存在的情况下生长和茁壮成长。关于外联和培训，该项目将为来自各种族裔和社会背景的不同群体的高中生、本科生和研究生提供研究培训机会。将通过与比利时、德国和波兰的同事进行国际研究交流和合作来加强对学生的培训，这些同事领导了欧洲ERA-CAPS(http://www.eracaps.org/)伙伴项目)，题为“促进对铝的遗传毒性的分子理解以促进作物改良”。最后，该项目将为一名来自当地学区的当地高中教师提供暑期研究培训实习机会，该学区为大量拉美裔学生提供服务。铝是地壳中储量最丰富的金属。在酸性环境中，铝会转化为剧毒的Al3+形式。虽然植物排斥铝的机制相对简单，但人们对铝毒害的生化基础以及铝导致严重的根生长抑制并对产量产生深刻影响的原因知之甚少。最近在模式植物拟南芥中的研究表明，铝可能作为一种遗传毒剂，通过铝触发细胞周期检查点通路而导致DNA损伤，该通路主要由细胞周期检查点因子共济失调、毛细血管扩张突变和Rad3相关(ATR)调节。具体地说，ATR的突变似乎通过抑制细胞周期进程而赋予植物实质性的耐铝性，细胞周期进程迫使根对铝的末端分化。铝作为DNA胁迫诱导物的发现代表了铝毒性研究的新视角，值得进一步研究。本项目的目的是利用转录学、系统发育、基因组和表型分析相结合的方法研究铝对大麦和拟南芥根生长的新影响。通过开发一种模型，在长期暴露于铝之后停止根的生长，预计这些信息将使利用检查站控制来赋予重要的经济作物耐铝性。通过该项目产生的所有数据和资源都将向公众开放。基因组、序列和蛋白质组数据集将通过一个联合体网站和公开可用的数据库访问，其中包括ArrayExpress(www.ebi.ac.uk/arrayExpress)和PROCE档案(蛋白质组学数据的http://www.ebi.ac.uk/pride/archive/))。生物材料(种子、质粒等)将根据要求提供。关键品系的种子也将存放在适当的储存中心，如拟南芥生物资源中心(ABRC)和诺丁汉拟南芥品系储存中心(NASC)，并通过这些中心传播。

PI: Paul Larsen (University of California-Riverside) ERA-CAPS Collaborators: Lieven DeVeylder (Ghent University, Belgium), Arp Schnittger (Hamburg University, Germany) and Iwona Szarejko (University of Silensia-Katowice, Poland) Aluminum (Al) toxicity is an important limitation to worldwide crop production, occurring in upwards of 50% of the world's arable land. The most evident symptom and important consequence of Al toxicity is root growth inhibition on acidic soils. A prominent example is barley, which is one of the most important crops in temperate regions including Europe and North America. Barley is very sensitive to Al toxicity and yield losses of up to 30% have been associated with growth in acidic soils. It has been previously argued that Al toxicity was an intractable problem due to its apparent complexity. The goal of this project is to define the biochemical mechanism that underlies inhibition of root growth in Arabidopsis and barley following chronic exposure to Al. It is the expectation that an inclusive understanding of this novel process will enable the development of agricultural crop plants that can grow and thrive in the presence of Al. With regard to outreach and training, this project will provide research training opportunities for a diverse group of high school, undergraduate and graduate students from a range of ethnic and social backgrounds. Student training will be enhanced by international research exchanges and collaborations with colleagues from Belgium, Germany and Poland who lead the European ERA-CAPS (http://www.eracaps.org/) companion project entitled "Towards a molecular understanding of aluminium genotoxicity for crop improvement (Al-UCIDATE)". Finally, the project will provide a summer research training internship for a local high school teacher from a local school district that serves a significant Hispanic student population. Aluminum is the most abundant metal in the earth's crust. When found in acidic environments, Al converts to the highly toxic Al3+ form. While the mechanisms of Al exclusion from plants are relatively simple, little is known about the biochemical basis of Al toxicity and why Al leads to severe root growth inhibition with profound effects on yield. Recent work in the model plant Arabidopsis thaliana has shown that Al may act as a genotoxic agent, with DNA damage caused by Al triggering a cell cycle checkpoint pathway that is regulated largely by the cell cycle checkpoint factor Ataxia telangiectasia mutated and RAD3-related (ATR). Specifically, mutations in ATR appear to confer substantial Al tolerance to the plant by suppressing cell cycle progression which forces terminal differentiation of the root in response to Al. The finding that Al acts as a DNA-stress inducing compound represents a new perspective on Al toxicity that bears further investigation. The goal of this project is to study this novel effect of Al on root growth in barley and Arabidopsis using a combination of transcriptomic, phylogenetic, genomic and phenotypic analyses. By developing a model by which root growth is halted following chronic exposure to Al, it is anticipated that the information will enable the exploitation of checkpoint control to confer Al tolerance to economically important crop plants. All data and resources generated through this project will be publicly accessible. Genome, sequence, and proteome datasets will be accessible through a consortium website and through publicly available data repositories that include ArrayExpress (www.ebi.ac.uk/arrayexpress) and the PRIDE Archive (http://www.ebi.ac.uk/pride/archive/) for proteomics data. Biological materials (seeds, plasmids, etc.) will be made available upon request. Seeds of key lines will also be deposited at and disseminated through the appropriate stock centers such as the Arabidopsis Biological Resource Center (ABRC) and Nottingham Arabidopsis Stock Centre (NASC) for Arabidopsis lines.