GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE319nnn/GSE319952/primaryOK200TranscriptomicsMus musculusExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE319952GEOGSEfalseRNA-seq analysis of Schwann cell knockout Bap1 and Kdm6b/Jmjd3Our previous studies have shown that Polycomb repression is responsible for repression of a latent regeneration program in Schwann cells that becomes activated after nerve injury. In particular, the Eed subunit of Polycomb Repressive Complex 2 is required to maintain repression of the injury program. Recently we have investigated the role of proteins that reverse polycomb repression : H3K27 demethylases and H2AK119ub1 deubiquitinases. While deletion of the KDM6B/JMJD3 H3K27 demethylase showed no major effect on Schwann cells, the deletion of the BAP1 deubiquitinase for PRC1-mediated H2AK119 monoubiquitination led to a progressive neuropathy at later time points.The modest phenotypes observed above, led us to hypothesize that these erasers, while enzymatically distinct, may function redundantly in a common gene regulatory pathway.. To test the potentially redundant function of the BAP1 and KDM6B/JMJD3 polycomb erasers, a Schwann cell-specific deletion of Bap1 and Kdm6b revealed a dramatic early onset phenotype after Schwann cell-specific deletion of these two genes, including a dramatic loss of myelinated axons. In addition, we find a deregulation of a larger subset of genes associated with H3K27me3 and H2AK119ub1 compared to either individual Schwann cell-specific knockout. Overall, our data support a model in which the proper maintenance of polycomb repression is dependent on the coordinate activities of the JMJD3 H3K27 demethylase and the BAP1 H2AK119 deubiquitinase.2026/09/01GSE319952GSM9530291GSM9530286GSM9530287GSM9530284GSM9530285GSM9530288GSM9530289GSM953029024247319952Mus musculus