SGER: Relationship Between Chemical Mutagenesis, Mutation Load, and Cell Cycle in Plants

This project aims to bring an understanding to the relationship between chemical mutagen treatment, M1 seedling survival, mutation load and cell cycle in plants. Traditional methods rely on survival of treated seedlings as the major determinant to mutation load carried in subsequent populations. However, results in various plant species indicate that this measure is not a good predictor leading to the development of reverse genetic collections with low mutation loads complicating the high throughput screening process. It is hypothesized that application of chemical mutagens at a critical time point, determined by a measure of cell cycle in fast growing vegetative versus slow growing reproductive tissue, may result in development of populations carrying higher mutation load. These molecular predicators can then be applied to any plant species for development of valuable reverse genetic collection.

The challenge for the post-sequencing era is to identify the biological functions of sequenced genes. Reverse genetics - the discovery of specific genes by searching for lesions responsible for observed disruptions in phenotype -plays an essential role in that process. The large, complex genomes of important crop species necessitate the development of a large number of mutants, and genetic screening methods developed to date do not support the high throughput necessary for making this search efficient. The goal is to identify the factors critical to the development of these populations in plants. Such understanding may allow better manipulation of crops to sustain an ever-increasing world population. Phenotypic, genetic, and molecular characterization of mutants provides an excellent tool for teaching students. Thus, research activities and outcomes of this project will be interfaced with programs designed to recruit and train students at all levels. Project outcomes will be disseminated through publications in peer-reviewed journals.