Hedgehog (Hh) and TGF-beta are crucial signaling pathways in embryonic development. Hh signaling relies on the primary cilium, an organelle that is present on nearly all mammalian cells. Cell-cycle related kinase (CCRK) phosphorylates a second kinase, Intestinal cell kinase (ICK) and both proteins have roles in ciliogenesis and ciliary length regulation. In the first part of this work, the synergistic relationship between CCRK and ICK is explored in the context of Hh-controlled vertebrate tissue patterning and ciliogenesis. Ccrk-/-Ick-/- double mutant embryos were found to have more severe phenotypes than Ccrk-/- and Ick-/- embryos in neural tube and limb bud patterning. Additionally, abnormal left-right (L-R) patterning is a new phenotype that is observed in double mutants. Double mutants showed a more severe phenotype in ciliogenesis when analyzing the ability of centrioles to generate cilia. My findings reveal independent roles for each kinase and functional overlap between these roles.The second part of this work focuses on TGF-beta signaling, which is required for organogenesis and early patterning events. One example is the crucial TGF-beta ligand, Nodal, in L-R patterning. The processing and secretion of Nodal is a complicated process that influences early L-R patterning. In my studies, the role of Rab23 is investigated in the context of L-R patterning and Nodal subcellular localization, processing, and secretion. Rab23 was previously shown to function in L-R patterning, but the mechanism of action was elusive. Here, I show that Rab23 controls Nodal secretion, acting in the latter part of the Nodal secretory pathway. Loss of Rab23 causes an accumulation of Nodal in Rab8+ vesicles, indicating perturbed exocytosis. Furthermore, our results point to an instructive role for Rab23 in node cells to drive asymmetric Nodal secretion in response to biophysical information (mechanociliary bending by leftward fluid flow).