Neurogenesis is a highly regulated process that results in the emergence of diverse neural cell types from progenitor and stem cell pools. The RE 1-silencing transcription factor (REST) has been proposed to play a role in regulating neurogenesis, fine-tuning expression of neural genes, and suppressing expression of target genes in non-neural tissues. REST is a part of a neuronal macro-repressor complex. REST acts by binding to a highly conserved DNA element, the RE1 site; once bound, it recruits co-repressors Sin3 to its N-terminal domain and the CoREST family to its C-terminal domain, which subsequently recruit chromatin modifiers to form the repressor complex. Initially, CoREST was identified in association to the REST complex, but it is now recognized that CoREST also works independent of REST. In vertebrates, the CoREST family contains three members, RCOR1, RCOR2, and RCOR3; distinct activities and roles have yet to be established for each of these proteins. To tease apart the REST-dependent and REST-independent roles of the CoREST family in neural development, we used transcription activator-like effector nucleases (TALENS) to disrupt all three CoREST genes in zebrafish. The three single mutants and all three double mutant combinations are viable. qPCR analysis revealed that expression levels of RE1- containing genes differs between the CoREST mutants, suggesting unique roles for each protein. In addition, analysis of larval locomotor behavior of each of the mutants revealed distinct behaviors were produced in the absence of each CoREST gene. These results show that members of the CoREST family differentially mediate gene expression and larval behavior and suggest both redundant and unique functions for zebrafish CoREST family members during development.