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PRC1 在没有 PRC2 功能的情况下维持神经命运的完整性。

PRC1 sustains the integrity of neural fate in the absence of PRC2 function.

机构信息

Neuroscience Institute, Department of Neuroscience and Physiology, NYU School of Medicine, New York, United States.

Department of Biology, New York University, New York, United States.

出版信息

Elife. 2022 Jan 7;11:e72769. doi: 10.7554/eLife.72769.

DOI:10.7554/eLife.72769
PMID:34994686
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8765755/
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 in mice leads to increased chromatin accessibility and ectopic expression of a broad variety of fates determinants, including transcription factors, while neuronal class-specific features are maintained. Loss of MN subtype identities in mutants is due to the suppression of Hox-dependent specification programs by derepressed paralogs (, , , ). 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.

摘要

多梳抑制复合物 (PRC) 1 和 2 通过建立基因抑制的可遗传模式，维持早期命运决定的稳定细胞记忆。PRC 通过组蛋白修饰和染色质紧缩来抑制转录，但它们在神经元亚型多样化中的作用尚未明确界定。我们发现 PRC1 对于节段性限制的脊髓运动神经元 (MN) 亚型的特化是必不可少的，而 PRC2 的活性在 MN 位置身份的终末分化过程中是可有可无的。在小鼠中核心 PRC1 成分的突变导致染色质可及性增加和广泛的各种命运决定因素（包括转录因子）的异位表达，而神经元类特异性特征得以维持。在 突变体中 MN 亚型身份的丧失是由于去抑制的 同源物（,,, ）抑制了依赖 Hox 的特化程序。这些结果表明，PRC1 可以在缺乏新生成的 PRC2 依赖性组蛋白甲基化的情况下发挥作用，以维持染色质拓扑结构和有丝分裂后神经元命运。

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