LncRNA is a regulator for harmonizing maturity and resilient functionality in spinal motor neurons.

Long noncoding RNAs (lncRNAs) play pivotal roles in modulating gene expression during development and disease. Despite their high expression in the central nervous system (CNS), understanding the precise physiological functions of CNS-associated lncRNAs has been challenging, largely due to the -centric nature of studies in this field. Here, utilizing mouse embryonic stem cell (ESC)-derived motor neurons (MNs), we identified an unexplored MN-specific lncRNA, (ong nergenic RNAs in at ntron). By employing an "exon-only" deletion strategy in ESCs and a mouse model, we reveal that deletion profoundly impacts MN dendritic complexity, axonal growth, and altered action potential patterns. Mechanistically, voltage-gated channels and neurite growth-related genes exhibited heightened sensitivity to deletion. Our -knockout mouse model displayed compromised motor behaviors and reduced muscle strength, highlighting 's critical role in motor function. This study unveils an underappreciated function of lncRNAs in orchestrating MN maturation and maintaining robust electrophysiological properties.