The transcription factor Tbx5 is necessary for development of the forelimb and closely linked with the evolution of this limb. Loss of just one copy of TBX5 in humans is associated with Holt-Oram Syndrome (HOS), which manifests as defects in both the forelimb and the heart. In zebrafish, tbx5 was duplicated during the teleost specific whole-genome duplication, and zebrafish therefore have two copies of tbx5: tbx5a and tbx5b. In the pectoral fins of wildtype embryos, the cells of the fin field migrate away from the somites along the mediolateral (ML) axis and converge along the anterio-posterior (AP) axis. Tbx5a regulates the AP convergence of these cells during fin field migration by controlling expression of fgf24 in a subset of the fin field cues. Therefore, loss of Tbx5a results in embryos lacking pectoral fins. Tbx5b-deficient embryos form small pectoral fins, through unknown mechanisms. In this dissertation, I aim to characterize the role of tbx5b during zebrafish development, particularly during pectoral fin development, and compare to the known functions of tbx5a. These comparisons will provide insight into the fate of duplicated genes in the zebrafish. All previous work on the role of tbx5b has been performed in Tbx5b-deficient embryos generated via morpholino. In order to confirm that the morpholino accurately recapitulates the mutant phenotype, I first created and characterized a mutant for tbx5b. The tbx5b -/- embryos phenocopy the previously described Tbx5b-deficient embryos in both the heart and the pectoral fin defects. Further analysis of tbx5b -/- pectoral fins reveals that in addition to the small size when compared to same-stage wildtype fins, tbx5b -/- pectoral fins lack some anterior structures of the fin, which is similar to the limb defects seen in HOS patients. In order to identify the different transcriptional networks of embryos deficient in the tbx5 paralogues, whole-embryo RNA sequencing was performed in wildtype embryos and embryos lacking the tbx5 paralogues during the stages of pectoral fin development. Loss of the tbx5 paralogues, in particular tbx5b, resulted in changes to gene expression in the intermediate mesoderm, the somites, and the yolk syncytial layer, which may be sources of signaling cues during the migration processes of the cells of the fin field, due to their proximity to the migrating cells. Furthermore, loss of the tbx5 paralogues produced morphological changes in both the vasculature and the somites. To understand how loss of tbx5b could result in a small fin, I performed cell tracking analysis in the fin field of Tbx5b-deficient embryos and compared this data to previously collected data on the dynamics of the cells of the fin field in both wildtype and Tbx5a- deficient embryos. Normal fin field migration involves both an AP convergence movement and a ML migration. In Tbx5a-deficient embryos, the signaling molecule Fgf24 is no longer present, resulting in a lack of AP convergence, although ML migration is unaffected. In Tbx5b-deficient embryos, there are mild defects in AP convergence, likely due to a decrease in the levels of fgf24 expression. The anterior cells are most strongly affected by loss of Tbx5b, which may explain the anterior defects seen in Tbx5b-deficient fins. Additionally, in Tbx5b-deficient embryos, there is no net ML migration of the fin field. Furthermore, the double-deficient embryos display defects in both AP convergence and ML migration. Overall, this dissertation expands the knowledge on the role of the tbx5 paralogues in zebrafish during migration of the cells of the fin field. Loss of the tbx5 paralogues results in changes in surrounding tissues, illustrating the complex interactions and signaling that occur between tissues. Likewise, tissues such as the intermediate mesoderm and yolk syn- cytial layer have the ability to impact the development of the fin. Additionally, both tbx5 paralogues regulate the migration of the cells of the fin field, with tbx5a primarily respon- sible for regulating AP convergence and tbx5b primarily responsible for regulating the ML migration movements. The genetic association of these movements along orthogonal axes suggests that subfunctionalization of these movements has occured. Furthermore, this data suggests that in tetrapods, the ancestral Tbx5 regulates both migration movements, such that loss of Tbx5 would result in cells that fail to migrate, therefore explaining the lack of forelimb in Tbx5-deficient tetrapods.