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.

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Iowa State University
United States
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