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<p>Chromatin must remain competent for responding rapidly to stress signals. Polycomb repressive complex 1 (PRC1) contributes to chromatin compaction through mono-ubiquitylation of histone H2A at Lys119 (H2AK119ub), yet how PRC1 complexes are dissociated from chromatin is only incompletely understood. Here, we show that the protease CAPN3 promotes rapid dissociation of PRC1 complexes from chromatin in response to stress. Following liver injury or heat shock, CAPN3 becomes activated and proteolyzes non-core PRC1 subunits to release the complexes from chromatin, leading to a reduction of H2AK119ub levels. These findings demonstrate that CAPN3 facilitates the remodeling of the chromatin landscape, unveiling a protease-mediated epigenetic mechanism for chromatin remodeling, and reveal CAPN3 as a key regulator of stress-induced epigenetic responses.</p>

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Protease-mediated PRC1 dissociation promotes H2AK119ub remodeling during stress responses

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年3月11日

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  • Wei Cui,
  • Qingyang Li,
  • Jinsong Wei,
  • Ting Zhou,
  • Haozhe Zhu,
  • Delai Huang,
  • Shuai Wang,
  • Jianan Gao,
  • Ru Zhou,
  • Zeyu Sun,
  • Hua Ruan,
  • Li Jan Lo,
  • Ting Tao,
  • Jun Chen,
  • Jinrong Peng,
  • Hui Shi

摘要

Chromatin must remain competent for responding rapidly to stress signals. Polycomb repressive complex 1 (PRC1) contributes to chromatin compaction through mono-ubiquitylation of histone H2A at Lys119 (H2AK119ub), yet how PRC1 complexes are dissociated from chromatin is only incompletely understood. Here, we show that the protease CAPN3 promotes rapid dissociation of PRC1 complexes from chromatin in response to stress. Following liver injury or heat shock, CAPN3 becomes activated and proteolyzes non-core PRC1 subunits to release the complexes from chromatin, leading to a reduction of H2AK119ub levels. These findings demonstrate that CAPN3 facilitates the remodeling of the chromatin landscape, unveiling a protease-mediated epigenetic mechanism for chromatin remodeling, and reveal CAPN3 as a key regulator of stress-induced epigenetic responses.