TY - JOUR TI - PRC1 sustains the integrity of neural fate in the absence of PRC2 function AU - Sawai, Ayana AU - Pfennig, Sarah AU - Bulajić, Milica AU - Miller, Alexander AU - Khodadadi-Jamayran, Alireza AU - Mazzoni, Esteban O AU - Dasen, Jeremy S A2 - Kratsios, Paschalis A2 - Bronner, Marianne E A2 - Kratsios, Paschalis VL - 11 PY - 2022 DA - 2022/01/07 SP - e72769 C1 - eLife 2022;11:e72769 DO - 10.7554/eLife.72769 UR - https://doi.org/10.7554/eLife.72769 AB - Polycomb repressive complexes (PRCs) 1 and 2 maintain stable cellular memories of early fate decisions by establishing heritable patterns of gene repression. PRCs repress transcription through histone modifications and chromatin compaction, but their roles in neuronal subtype diversification are poorly defined. We found that PRC1 is essential for the specification of segmentally restricted spinal motor neuron (MN) subtypes, while PRC2 activity is dispensable to maintain MN positional identities during terminal differentiation. Mutation of the core PRC1 component Ring1 in mice leads to increased chromatin accessibility and ectopic expression of a broad variety of fates determinants, including Hox transcription factors, while neuronal class-specific features are maintained. Loss of MN subtype identities in Ring1 mutants is due to the suppression of Hox-dependent specification programs by derepressed Hox13 paralogs (Hoxa13, Hoxb13, Hoxc13, Hoxd13). These results indicate that PRC1 can function in the absence of de novo PRC2-dependent histone methylation to maintain chromatin topology and postmitotic neuronal fate. KW - neural development KW - motor neuron KW - hox gene KW - polycomb protein JF - eLife SN - 2050-084X PB - eLife Sciences Publications, Ltd ER -