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Plants are important for human survival and the environment. They provide oxygen, food, medicine and fuel. Understanding the development of plants has been a fundamental research question. Among all the plant tissues, the most important ones are the meristems. Sitting at the tip of the shoot and the root are the shoot apical meristem (SAM) and the root apical meristem (RAM). The shoot apical meristem gives rise to the above-ground organs like leaves and flowers while the root apical meristem produces all the root tissues that help to anchor the plants and transport water and nutrients. As the meristem is capable of producing new organs throughout the lifespan of a plant, the study of meristem maintenance and development provides the key to the understanding of plant development.Arabidopsis transcription factor TSO1 plays an essential role for the proper development of shoot apical meristem and root apical meristem. TSO1 encodes a protein with a cysteine-rich repeats domain and TSO1 is a potential component of a cell cycle regulating complex, the DREAM complex. The tso1-1 mutant has fasciated SAM due to shoot meristem cell over-proliferation and complete sterility due to lack of differentiated female and male floral organs. Interestingly, the tso1-1 mutant also produces shorter root than the wild type, presumably caused by early differentiation of the cells in the RAM. A prior mutagenesis screen identified two major suppressors of tso1-1. Characterization of these tso1-1 suppressor mutations provides important insights to the understanding of TSO1-regulatory pathways. My dissertation project focuses on analyzing one of these suppressors that was shown to be a mutated type-A cyclin gene named CYCA3;4. Mutations in CYCA3;4 suppress the shoot phenotype but not the root phenotype of tso1-1. The suppressed plants can produce normal floral organs and become partially fertile. Using transgenic method, I showed that the expression of CYCA3;4 was increased in the tso1-1 SAM, and overexpression of CYCA3;4 in the tso1-3 mutant enhanced the fertility defect, suggesting that overexpression of CYCA3;4 partially mediates the tso1-1 shoot phenotype. In addition, I provided evidence supporting that TSO1 likely represses CYCA3;4 gene expression indirectly through MYB3R1, whose mutations also suppress tso1-1 mutants. My dissertation provides an important link between TSO1, a potential cell cycle regulatory complex component and meristem regulator, and cyclin A, a protein directly involved in cell cycle regulation. This link provides an important mechanistic insight into how plant meristems maintain their identity by limiting their cell division activity. To further investigate the mechanism of TSO1 action in the root, I collaborated with two other scientists to profile the gene expression in the tso1-1 root at single cell level. I compared the single cell RNA sequencing data of tso1-1 and wild type roots and identified molecular defects in the tso1-1 root vasculature. Correspondingly, the known regulators of vasculature development, the HD-ZIP III genes, are ectopically expressed in some of the vascular cells in the tso1-1 root. It suggests that the defects of root vasculature may be attributed to mis-expressed HD-ZIP III genes in the tso1-1 mutant. The HD-ZIPIII function was previously linked to their regulation of cytokinin biosynthesis genes, which were ectopically expressed in tso1-1 roots as revealed by our scRNA-seq data. Together, our data suggest that the over-production of cytokinin might be the cause of tso1-1 short root phenotype. In summary, my dissertation research revealed previously unknown links between TSO1 and cell cycle regulation in the shoot and root meristems as well as the molecular mechanisms of TSO1 function in the root vascular development at single cell level. These findings have furthered our understanding of how cell cycle regulation is integrated with plant development.