During mammalian neurodevelopment, the establishment of spatial and temporally appropriate gene expression programmes ensures the correct production of distinct neural and glial cell types. This process is partially regulated by the modification of chromatin structure by epigenetic complexes, including the Polycomb group (PcG) family of co-repressors. Genetic screening has identified several PcG mutations that are causally associated with a range of congenital brain disorders, yet the specific regulatory roles of Polycomb complexes during normal neurodevelopment is still unclear. Here, we investigate the effect of catalytically deficient Polycomb repressive complex 1 (PRC1) (Ring1BI53A/I53A) during mouse embryonic neurodevelopment. We show during neural differentiation of mouse embryonic stem cells (ESCs) that reduced PRC1 catalytic activity derepresses non neuroectoderm-associated genes, coinciding with a significant loss of H2AK119ub. Similar gene expression patterns were found in ex vivo neural stem cells derived from WT and Ring1BI53A/I53A embryos and this was further verified at a protein level by mass spectrometry. Looking in vivo at embryonic day 12.5, we show reduced overall body size, reduced cortical thickness and a reduction in key developmental markers. Taken together, this study furthers our understanding of the function for RING1B in regulating early neural differentiation.