Cohesin and NuRD Antagonistically Drive Alternative Neuronal Fates via PLZF Transcription Factors
This study reveals that in *C. elegans*, cohesin and the PLZF homolog EOR-1 promote GABAergic neuronal fate, while the NuRD complex and another PLZF homolog (TRA-4) drive an alternative tyraminergic fate when cohesin function is lost, demonstrating an antagonistic mechanism where genome architecture, epigenetic remodeling, and transcriptional regulation cooperate to specify neuronal identity.