@article{628d354656d949edad09ec7311108b1a,
title = "PRC1 sustains the integrity of neural fate in the absence of PRC2 function",
abstract = "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 main-tained. 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 methyla-tion to maintain chromatin topology and postmitotic neuronal fate.",
keywords = "Animals, Animals, Genetically Modified, Chickens, Embryonic Stem Cells/metabolism, Gene Expression Regulation, Developmental, Mice, Motor Neurons/metabolism, Polycomb Repressive Complex 1/genetics, Polycomb Repressive Complex 2/genetics",
author = "Ayana Sawai and Sarah Pfennig and Milica Bulaji{\'c} and Alexander Miller and Alireza Khodadadi-Jamayran and Mazzoni, {Esteban O.} and Dasen, {Jeremy S.}",
note = "Funding Information: We thank Kristen D?Elia, Sara Fenstermacher, Jessica Treisman, and Ed Ziff for discussion and comments on the manuscript, and Rachel Kim and Orly Wapinski for assistance. We thank Isabel Hidalgo and Susana Gonzalez for providing Ezh1flox/flox mice, Alexander Tarakhovsky for Ezh2flox/flox mice, Stefan Thor for Eed mutant embryos, Haruhiko Koseki for Ring1-/-::Rnf2flox/flox ES cells, and Robert Klose for Rybyflox/ flox::Yaf2-/- ES cells. We also thank Genome Technology Center and Cytometry and Cell Sorting Laboratory at NYU Langone. This work was supported by NIH NINDS grants T32 GM007238, F31 NS087772 to AS, R01 NS 100897 to EOM, R35 NS116858, R01 NS062822 and R01 NS097550 to JD. Funding Information: We thank Kristen D{\textquoteright}Elia, Sara Fenstermacher, Jessica Treisman, and Ed Ziff for discussion and comments on the manuscript, and Rachel Kim and Orly Wapinski for assistance. We thank Isabel Hidalgo and Susana Gonzalez for providing Ezh1flox/flox mice, Alexander Tarakhovsky for Ezh2flox/flox mice, Stefan Thor for Eed mutant embryos, Haruhiko Koseki for Ring1-/-::Rnf2flox/flox ES cells, and Robert Klose for Rybyflox/ flox::Yaf2-/- ES cells. We also thank Genome Technology Center and Cytometry and Cell Sorting Laboratory at NYU Langone. This work was supported by NIH NINDS grants T32 GM007238, F31 NS087772 to AS, R01 NS 100897 to EOM, R35 NS116858, R01 NS062822 and R01 NS097550 to JD. Publisher Copyright: {\textcopyright} Sawai et al.",
year = "2022",
month = jan,
doi = "10.7554/eLife.72769",
language = "English (US)",
volume = "11",
journal = "eLife",
issn = "2050-084X",
publisher = "eLife Sciences Publications",
}