REGULATORY NETWORKS THAT CONTROL AUTOPHAGY TO ENABLE ENVIRONMENTAL STRESS RESILIENCE IN PLANTS

这项研究将确定植物对不利环境条件做出反应并生存下来的细胞机制；这些机制是植物生存和生产力的关键。无论是在自然环境中，还是在农业环境中，植物经常遇到干旱、高温和洪水等环境胁迫。应激期间细胞存活的一个主要途径被称为自噬，在自噬过程中，受损的细胞成分被消化和回收，防止它们的有毒物质积累。关于自噬过程本身的大量信息是可用的，但自噬是如何被植物中的环境胁迫激活的还不清楚。这项研究将通过确定控制自噬的因素并确定它们在压力耐受中的作用来解决这个问题。这可能会导致新的方法来提高作物的抗逆性，从而促进它们的生长和产量。该项目将对博士后科学家、研究生和本科生进行研究技能和科学交流方面的培训。它还将通过对研究论文的注释来增加本科生对细胞生物学科学文献的可及性，这些研究论文可用于细胞生物学课程，并将在网上与科学界广泛分享。这一注释的有效性将通过干预前和干预后的有效调查来评估，以衡量学生自我效能、能力和动机信念的增加。自噬的激活是植物对环境胁迫反应的关键组成部分，被认为通过与其他胁迫反应协调的复杂途径来调节，以优化植物的生长和生存。尽管自噬起着关键作用，但在植物中还很少发现和表征自噬的调控因子。这个项目的目标是确定之前未描述的调节植物自噬的途径，这些途径既有转录作用，也有翻译后作用。我们将评估在不同条件下涉及蛋白激酶SnRK1的磷酸化级联反应控制自噬的机制，并确定一系列控制自噬基因表达的转录因子的功能，其中一些转录因子可能受SnRK1调控。这将通过遗传学方法来评估不同胁迫条件下因素之间的自噬和上位性功能，潜在磷酸化位点的突变，磷酸蛋白质组分析，以及最终整合磷酸化和转录激活事件的调控网络的构建。反过来，调控网络分析将使我们能够开始解决这些途径如何与其他胁迫信号途径整合和合作，以使植物在不利和不断变化的条件下具有韧性和生存能力。这一奖项反映了NSF的法定使命，并通过使用基金会的智力优势和更广泛的影响审查标准进行评估，被认为值得支持。

This research will identify cellular mechanisms by which plants respond to and survive adverse environmental conditions; these mechanisms are key to their survival and productivity. Plants frequently encounter environmental stresses, such as drought, heat and flooding, both in their natural environment and in the field in agricultural settings. A major pathway for cell survival during stress is called autophagy, in which damaged cell components are digested and recycled, preventing their toxic accumulation. Substantial information about the autophagy process itself is available, but how autophagy is activated by environmental stress in plants is not yet clear. This research will address this problem by identifying factors that control autophagy and determining their function in stress tolerance. This potentially will lead to new approaches to improve stress tolerance in crop plants, thus enhancing their growth and yield. The project will train a postdoctoral scientist, a graduate student, and undergraduate students in research skills and scientific communication. It will also increase the accessibility of the cell biology scientific literature to undergraduates by annotation of research papers, which can be used in cell biology classes and will be shared broadly online with the scientific community. The effectiveness of this annotation will be assessed using validated pre- and post-intervention surveys to measure student increases in self-efficacy, competence and motivational beliefs.The activation of autophagy is a key component of plant responses to environmental stress, and is thought to be regulated via complex pathways that are coordinated with other stress responses to optimize plant growth and survival. Despite this critical role, very few regulatory factors for autophagy have yet been identified and characterized in plants. The goal of this project is to identify previously undescribed pathways for the regulation of autophagy in plants that act both transcriptionally and post-translationally. We will assess the mechanisms by which phosphorylation cascades involving the protein kinase SnRK1 control autophagy under different conditions, and determine the function of a suite of transcription factors that control autophagy gene expression, some of which are potentially regulated by SnRK1. This will be accomplished by genetic approaches to assess function in autophagy and epistasis among factors under different stress conditions, mutation of potential phosphorylation sites, phosphoproteomic analysis, and finally the construction of regulatory networks that integrate both phosphorylation and transcriptional activation events. The regulatory network analysis will in turn allow us to begin addressing how these pathways integrate and cooperate with other stress signaling pathways to enable plant resilience and survival in the face of adverse and changing conditions.This award reflects NSF's statutory mission and has been deemed worthy of support through evaluation using the Foundation's intellectual merit and broader impacts review criteria.