All plants grow from stem cells or a collection of stem cells organized at meristems. The activity and function of these meristems determine plant morphology. In shoots, development at the Shoot Apical Meristem (SAM) determines the rate and position of lateral organ formation, the transition from vegetative to reproductive growth, and the overall branching architecture. SAMs accomplish these functions while maintaining themselves and simultaneously producing cells incorporated into lateral organs. Decades of research in the model plant Arabidopsis thaliana has revealed numerous mechanisms at play regulating meristem function. A negative feedback loop between the indeterminacy promoting transcription factor WUSCHEL (WUS), the secreted peptide CLAVATA3 (CLV3), and a series of LEUCINE-RICH REPEAT RECEPTOR-LIKE KINASEs (LRR-RLKs) that inhibit WUS comprises the canonical network governing SAM maintenance. WUS is induced by the phytohormone cytokinin, which is in turn regulated by crosstalk from another phytohormone: auxin. Altogether, a complex regulatory network composed of WUS, CLV3, LRR-RLKs, cytokinin, and auxin regulates the function of the SAM. Our understanding of SAM function is limited outside of Arabidopsis and a few crops. However, even anatomically and evolutionarily disparate SAMs must perform the same functions as those in angiosperms. For example, whereas diploid flowering plant SAMs are multicellular structures organized into distinct clonal layers and different functional domains, the haploid shoot of the moss Physcomitrium patens is derived from a single tetrahedral apical cell. This apical cell nonetheless produces leaves (phyllids) in a spiral phyllotactic pattern while maintaining itself until it establishes the site of reproductive organ formation. In my dissertation work, I sought to elucidate whether the mechanisms regulating the function of this single celled meristem parallel those in the flowering plant SAM. I took a reverse-genetics approach and assessed the function of moss LRR-RLK genes CLAVATA1a (CLV1a), CLV1b, and RECEPTOR-LIKE PROTEIN KINASE2 (RPK2), which are orthologs of LRR-RLKs that inhibit WUS in Arabidopsis. I found that these LRR-RLK genes performed the same developmental function in moss as in flowering plants, namely the inhibition of stem cell specification. Fascinatingly, published data suggest that WUSCHEL-RELATED HOMEOBOX (WOX) genes do not function in regulation of the moss SAM, leading me to ask how CLV1 and RPK2 function in moss if not by inhibiting WUS. In both moss and flowering plants, cytokinin promotes SAM specification and function while CLV1 and RPK2 inhibit them. Given the absence of a WOX gene from moss stem cell regulation I tested whether there is crosstalk between cytokinin and CLV1/RPK2. Using a combination of genetics, hormone treatments, and mathematical modeling, I provide support for a model where CLV1 acts upstream of cytokinin-mediated SAM specification while RPK2 acts in a distinct pathway. Next, by combinatorically increasing and decreasing auxin and cytokinin signaling, I show that the ratio of auxin to cytokinin signaling also governs moss shoot morphogenesis. Overall, this work supports the conclusion that similar mechanisms support SAM function in mosses and flowering plants, despite the independent evolution of these shoots over four hundred million years ago. To support future evolutionary and developmental work on this topic, my final contribution is a phylogenetic analysis and functional summary of stem cell-regulating LRR-RLKs. In total, I hope that this work contributes to a general understanding of the developmental mechanisms at play across the land plant tree of life.