Here I recount five stories describing the function of several key genes in plant development. Much of this work focuses on the role of the kinases TARGET OF RAPAMYCIN (TOR). TOR is the focus of many researchers interested in metabolic diseases and cancers since TOR dysregulation is a major cause of such diseases. The role of TOR in plants is relatively unexplored, however, and questions surrounding its upstream cues and downstream targets persist. TOR is a deeply conserved Ser/Thr protein kinase that integrates an array of metabolic processes to coordinate growth and development with nutritional status in eukaryotes. TOR is often dysregulated in many human diseases including diabetes and cancer, and as such, has been relatively well studied in mammalian systems. The TOR protein and complex are well-conserved across the eukaryotic kingdom; however, their role in plant growth and development is not as well understood. Recent work in this emerging field has shown that TOR plays a similar role in plants, serving as a metabolic rheostat modulating developmental processes in response to signals like light, sugars, and phosphorus abundance. In response, TOR regulates key pathways like nucleotide biosynthesis, ribosome biogenesis, and leaf initiation. In chapter 2, I detail a series of experiments aimed at teasing out TOR’s role in sensing and responding to nucleotide availability in plants. I performed a functional genetic screen to identify genes that affect TOR activity in Nicotiana benthamiana. I identified a key regulatory enzyme, cytosolic phosphoribosyl pyrophosphate (PRPP) synthetase (PRS4), that catalyzes the conversion of ribose-5-phosphate into PRPP, an upstream metabolite in nucleotide synthesis and salvage pathways. I showed that prs4 knockdowns show reduced phosphorylation of S6K, a hallmark of reduced TOR activity, and prs4 knockouts are embryo-lethal in A. thaliana. Furthermore, silencing PRS4 expression caused pleiotropic developmental phenotypes in Nicotiana plants while RNA-Seq analysis revealed that ribosome biogenesis was one of the most strongly repressed processes. I then fused a chemical genetic approach and found that TOR activity is impaired by disruption of nucleotide biosynthesis and confirmed this by knocking down other genes in the nucleotide biosynthesis pathways. I found that this effect can be reversed by supplying plants with nucleobases and physiological levels of nucleotides. Finally, I surveyed publicly available transcriptomic data and found TOR transcriptionally promotes nucleotide biosynthesis to support the demands of ribosomal RNA synthesis. In chapter 3, I explore the roles of an RNA-binding protein (RBP), TERMINAL EAR1 (TE1), in regulation of leaf initiation in maize and describe the embryo rescue system I designed to study TOR activity in maize seedlings. TE1 is a repressor of leaf initiation in maize, since mutants without TE1 produce nearly twice as many leaves compared to wild-type. TE1 is a member of a protein family named after the yeast homolog Mei2p. In yeast, the Mei2p is phosphorylated under nutrient-sufficient conditions, leading to its proteasomal degradation. I used the Te1 and mei2 sequences to identify other plant Mei2p-like proteins and used viral induced gene silencing to study their function. Then, with the assay I developed to toggle TOR activity and TE1 stability in maize seedlings, I began to explore how TE1 impacts genome expression in a preliminary RNA-Seq study. These data laid the groundwork for my postdoctoral research in which I will continue to explore the effects of Te1 expression on the leaf initiation regulatory network. In chapter 4, I outline a maize genetics experiment I performed to explore the genetic interaction of three genes: Terminal ear1, Phytochrome B1 (PhyB1), and Phytochrome B2 (PhyB2). While Terminal ear1 negatively regulates the initiation of new leaves, Phytochrome B1, and Phytochrome B2 redundantly promote leaf initiation, as phyB1; phyB2 double mutants have fewer leaves than wild-type. I crossed these distinct mutants to create a F2 population segregating for these three genes. The number of leaves in the triple mutant was between the extremes of the two parents, suggesting an additive genetic interaction between these genes. The phyB1; phyB2 double mutant exhibited a dramatic environmental response between greenhouse and field trials. The triple mutant showed a similar environmental response as well. Together, these data begin to outline the effects and interactions of key players in a gene regulatory network controlling leaf initiation in maize. Finally, in chapter 5 I summarize another maize genetics experiment in which I aimed to identify inbred-specific modifiers of the maize mutant narrow odd dwarf (nod). The maize mutant narrow odd dwarf (nod) exhibits defects in cell division, expansion, and differentiation resulting in leaves with fewer and smaller cells, delayed maturation, patterning defects, and shorter plants. The severity of these defects is dramatically different in different inbred backgrounds pointing to the existence of inbred-specific modifiers of the nod phenotype. I sought to map the modifiers of the nod phenotype by creating large F2 mapping populations from the nod mutants in each inbred line. I crossed the nod in B73 mutant to nod mutants in Mo17 and A619. I scored the individuals in the F2 and, due to the continuous distribution of phenotypes, found that there are likely many inbred-specific modifiers contributing to the inbred-differences phenotypic severity. I used DNA from these families for genotyping-by-sequencing to identify QTL associated with certain phenotypes. LIGULELESS NARROW (LGN) was found to interact with NOD in vivo and identified as a modifier of nod. The Lgn-R mutant was crossed to nod to create a Lgn; nod double mutant. I analyzed transcriptomic datasets for Lgn; nod, and the double mutant to identify similarities in their transcriptomes that may help explain their phenotypes. I found that the Lgn and nod transcriptomes were strikingly similar, despite phenotypic differences. My analysis of the double mutant revealed that these genes likely act in overlapping pathways to regulate maize development.