<p>Heterosis, or hybrid vigor, is a phenomenon observed in both plant and animal systems where hybrid offspring perform better when compared to their parents. For hybrid plants, this can result in increased biomass, crop yields, and vigor when compared to the inbred parents. Even though heterosis has been used in agriculture for over a century, the molecular mechanisms that result in hybrid vigor remain elusive even after years of investigation. A molecular understanding of heterosis is desirable because it will speed up the process of breeding compatible inbred lines for developing hybrid seeds, and it will provide us with the knowledge to potentially engineer inbred lines that can mimic the beneficial phenotypic effects of heterosis, eliminating the need for farmers to buy new hybrid seeds every year. The goal of this research project is to identify genes that are required for heterotic phenotypes in maize. Our working hypothesis is that a mutation in genes that are essential for heterosis will cause an altered heterotic phenotype in hybrid maize plants. To test this hypothesis, we applied combined approaches of EMS mutagenesis, trait phenotyping in field and controlled conditions, bulk segregant analysis, whole genome sequencing, and bioinformatics analysis. First, we applied a forward genetics approach to identify mutant hybrids with altered heterosis and detected potential causal genes <em>via</em> whole genome sequencing. We identified one mutation occurring in a protein coding gene (gene ID <em>Zm00001eb305590</em>) located in a region of interest on chromosome 7, whose genotypes across various samples assayed fit the observed segregation pattern of hybrid traits. This mutation leads to a moderate or high-level codon change, indicating that this gene may play a role in mediating heterosis in maize. By investigating this gene with further studies, the learned knowledge could speed up the process of hybrid maize breeding by selecting compatible inbred lines through sequencing or by engineering hybrids that have favorable alleles for this gene.</p>