In the genetic disorder familial dysautonomia (FD), mutations in elongator acetyltransferase complex subunit 1 (ELP1) cause severe nervous system phenotypes. Abnormal development of the trigeminal nerve results in decreased facial pain and temperature perception in FD, but the molecular mechanisms leading to these sensory deficits are poorly understood. Preliminary data from an FD mutant mouse model suggest loss of Elp1 increases expression of Pdlim7 and several proteins in the Yap1 signaling pathway. Pdlim7 promotes activation of Yap1 through direct binding in other contexts, but the role of Pdlim7 in trigeminal sensory neuron development has not been described. Furthermore, it is unclear how dysregulation of Yap1 through increased Pdlim7 expression may contribute to FD neuronal phenotypes. To address this, I characterized the normal expression of Pdlim7 and Yap1 in embryonic mouse trigeminal ganglion neurons. Through immunohistochemistry, I found that Pdlim7 is expressed in the cytoplasm of early trigeminal ganglion neurons. Yap1 is also expressed in several cell types, including some neurons, while the active form of Yap1 was enriched in neural crest cell precursors and placodal neurons. Using immunoblotting, I determined that Pdlim7 and Yap1 levels and activation change across developmental timepoints in trigeminal nerve target tissue. Co-expression and biochemical interaction of Pdlim7 and Yap1 indicates their potential role in trigeminal neurodevelopment. The results of this project have improved our understanding of the functions of Pdlim7 and Yap1 and provide a basis for further study of how altering Pdlim7 and Yap1 pathways may disrupt neurodevelopment in FD.