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PICKLE-mediated nucleosome condensing drives H3K27me3 spreading for the inheritance of Polycomb memory during differentiation
Molecular Cell ( IF 14.5 ) Pub Date : 2024-09-03 , DOI: 10.1016/j.molcel.2024.08.018 Zhenwei Liang 1 , Tao Zhu 1 , Yaoguang Yu 1 , Caihong Wu 1 , Yisui Huang 1 , Yuanhao Hao 1 , Xin Song 1 , Wei Fu 1 , Liangbing Yuan 1 , Yuhai Cui 2 , Shangzhi Huang 1 , Chenlong Li 1
Molecular Cell ( IF 14.5 ) Pub Date : 2024-09-03 , DOI: 10.1016/j.molcel.2024.08.018 Zhenwei Liang 1 , Tao Zhu 1 , Yaoguang Yu 1 , Caihong Wu 1 , Yisui Huang 1 , Yuanhao Hao 1 , Xin Song 1 , Wei Fu 1 , Liangbing Yuan 1 , Yuhai Cui 2 , Shangzhi Huang 1 , Chenlong Li 1
Affiliation
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Spreading of H3K27me3 is crucial for the maintenance of mitotically inheritable Polycomb-mediated chromatin silencing in animals and plants. However, how Polycomb repressive complex 2 (PRC2) accesses unmodified nucleosomes in spreading regions for spreading H3K27me3 remains unclear. Here, we show in Arabidopsis thaliana that the chromatin remodeler PICKLE (PKL) plays a specialized role in H3K27me3 spreading to safeguard cell identity during differentiation. PKL specifically localizes to H3K27me3 spreading regions but not to nucleation sites and physically associates with PRC2. Loss of PKL disrupts the occupancy of the PRC2 catalytic subunit CLF in spreading regions and leads to aberrant dedifferentiation. Nucleosome density increase endowed by the ATPase function of PKL ensures that unmodified nucleosomes are accessible to PRC2 catalytic activity for H3K27me3 spreading. Our findings demonstrate that PKL-dependent nucleosome compaction is critical for PRC2-mediated H3K27me3 read-and-write function in H3K27me3 spreading, thus revealing a mechanism by which repressive chromatin domains are established and propagated.
中文翻译：
PICKLE 介导的核小体凝聚驱动 H3K27me3 扩散，以实现分化过程中多梳记忆的遗传
H3K27me3 的传播对于维持动植物有丝分裂可遗传的 Polycomb 介导的染色质沉默至关重要。然而，Polycomb 抑制复合物 2 （PRC2） 如何访问扩散区域中未修饰的核小体以传播 H3K27me3 仍不清楚。在这里，我们在拟南芥中表明，染色质重塑剂 PICKLE （PKL） 在 H3K27me3 扩散中起特殊作用，以保护分化过程中的细胞身份。PKL 特异性定位于 H3K27me3 扩散区域，但不定位于成核位点，并与 PRC2 物理结合。PKL 的缺失会破坏 PRC2 催化亚基 CLF 在扩散区域的占据，并导致异常的去分化。PKL 的 ATP 酶功能赋予的核小体密度增加确保未修饰的核小体可被 PRC2 催化活性接近，以促进 H3K27me3 扩散。我们的研究结果表明，PKL 依赖性核小体压缩对于 PRC2 介导的 H3K27me3 在 H3K27me3 传播中的读写功能至关重要，从而揭示了抑制性染色质结构域建立和传播的机制。
更新日期：2024-09-03
中文翻译：
PICKLE 介导的核小体凝聚驱动 H3K27me3 扩散，以实现分化过程中多梳记忆的遗传
H3K27me3 的传播对于维持动植物有丝分裂可遗传的 Polycomb 介导的染色质沉默至关重要。然而，Polycomb 抑制复合物 2 （PRC2） 如何访问扩散区域中未修饰的核小体以传播 H3K27me3 仍不清楚。在这里，我们在拟南芥中表明，染色质重塑剂 PICKLE （PKL） 在 H3K27me3 扩散中起特殊作用，以保护分化过程中的细胞身份。PKL 特异性定位于 H3K27me3 扩散区域，但不定位于成核位点，并与 PRC2 物理结合。PKL 的缺失会破坏 PRC2 催化亚基 CLF 在扩散区域的占据，并导致异常的去分化。PKL 的 ATP 酶功能赋予的核小体密度增加确保未修饰的核小体可被 PRC2 催化活性接近，以促进 H3K27me3 扩散。我们的研究结果表明，PKL 依赖性核小体压缩对于 PRC2 介导的 H3K27me3 在 H3K27me3 传播中的读写功能至关重要，从而揭示了抑制性染色质结构域建立和传播的机制。
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