The study of synapse development has uncovered multiple factors that are implicated in neurotransmitter biosynthesis and neurotransmitter receptor clustering. However, the molecular mechanisms that control these processes, in a presynaptic and a postsynaptic cell, remain elusive. Leveraging the C. elegans neuromuscular system, this thesis unveils the role of UNC-30 (PITX), the homeodomain terminal selector of GABAergic motor neuron identity, in postsynaptic organization. We show that loss of unc-30 (PITX) or the short isoform of the synapse-organizing molecule madd-4B (Punctin/ADAMTSL) results in severe GABA receptor clustering defects in postsynaptic muscle cells. Mechanistically, we identify UNC-30 as a direct regulator of madd-4B. In addition, we uncover a repertoire of novel targets regulated by UNC-30, revealing its dual role as both an activator and repressor of gene expression in GABAergic motor neurons. Specifically, UNC-30 represses genes normally expressed in other neuron types. We also uncover that UNC-30 is continuously required, from embryonic development through adulthood, to maintain madd-4B and GABA biosynthesis gene (e.g., unc-25/GAD, unc-47/VGAT) expression. These findings support the concept of coordinated presynaptic and postsynaptic differentiation, ensuring effective neurotransmission. Altogether, this work uncovers a transcriptional co-regulatory strategy essential for synapse functionality, demonstrating how neuronal identity and synapse organization are coordinated. The findings are expected to resonate with the developmental biology community and the broader field of gene regulation, offering insights into fundamental questions regarding transcriptional control of cell identity and function. Beyond its developmental biology contributions, this study holds biomedical relevance, as UNC-30/PITX mutations have been associated with diseases such as the Axenfeld-Rieger syndrome.