Acute chromatin decompaction stiffens the nucleus as revealed by nanopillar- induced nuclear deformation in cells

• 成果类型: Article
• 署名作者: Mitra, Aninda; Cutiongco, Marie F. A.; Burla, Romina; Zeng, Yongpeng; Na, Qin; Kong, Mengya; Vinod, Benjamin; Nai, Mui Hoon; Hubner, Barbara; Ludwig, Alexander; Lim, Chwee Teck; Shivashankar, G. V.; Saggio, Isabella; Zhao, Wenting
• 署名单位: Nanyang Technological University; Sapienza University Rome; National University of Singapore; Nanyang Technological University; Nanyang Technological University; National University of Singapore; National University of Singapore; Swiss Federal Institutes of Technology Domain; ETH Zurich; Swiss Federal Institutes of Technology Domain; Paul Scherrer Institute; Nanyang Technological University
• 刊物名称: PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
• ISSN/ISSBN: 0027-11258
• DOI: 10.1073/pnas.2416659122
• 发表日期: 2025-05-13
• 关键词: trichostatin-a; cancer-cells; migration; lamin; decondensation; expression; mechanics; DYNAMICS; genome; lung

摘要

Chromatin architecture is critical in determining nuclear mechanics. Most studies focus on the mechanical rigidity conferred by chromatin condensation from densely packed heterochromatin, but less is known on how transient chromatin decompaction impinge on nucleus stiffness. Here, we used an array of vertically aligned nanopillars to study nuclear deformability in situ after chromatin decompaction in cells. The nucleus significantly stiffened within 4 h of chromatin decompaction but softened at longer timescales. This acute stiffening of the nucleus was underpinned predominantly by an increase in nucleus volume and nuclear import, and partially by enhanced lamin protein recruitment to the periphery. The coupling between nucleus stiffening and acute chromatin HT1080) due to the capacity to efficiently compact heterochromatin into foci that sustains nucleus deformability required for confined migration. Our work signals how rapid chromatin remodeling is a physiologically relevant pathway to modulate nucleus mechanics and cell migration behavior.