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Peer-reviewedCC BY-NC-SA 4.0Molecular Biology of the Cell

Transcriptional activity generates chromatin motion that drives nuclear blebbing

  • Kelsey Prince1,2
  • Nickolas Borowski1
  • Katie Lin1
  • Andy Li1
  • Andrew D. Stephens1,2
  1. 1Biology department, University of Massachusetts Amherst, Amherst, MA 01003
  2. 2Molecular and Cellular Biology, University of Massachusetts Amherst, Amherst, MA 01003
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Abstract

Abnormal nuclear blebbing is a hallmark of human diseases, including cancers and age-related disorders. Previous work has outlined that nuclear blebbing is due to an imbalance of nuclear strength resisting actin confinement and contraction. Independent of this balance, our recent work revealed that inhibiting RNA polymerase II (RNA Pol II) suppresses nuclear blebbing, but the mechanism remains unknown. Disruption of transcriptional activity through rapid degradation of RNA Pol II via an auxin-inducible degron suppresses nuclear blebbing. To more finely decrease and then restore transcriptional activity, we removed culture media serum and then added it back, respectively. Decreasing transcriptional activity decreases nuclear bleb formation, stability, and rupture, while returning transcriptional activity increases nuclear blebbing. These modulations of transcriptional activity did not alter the nuclear spring constant or actin confinement and contraction. Instead, we find that transcriptional activity regulates chromatin domain motion measured by mean square displacement (MSD) of chromatin domains labeled via transfected Cy3-dNTPs. Increasing chromatin domain motion using an established RAD51 inhibitor B02 resulted in increased nuclear blebbing. Thus, we reveal that transcriptional activity drives nuclear blebbing through chromatin motion.

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Cite

BibTeXRIS
BibTeX
@article{prince2026transcriptional,
  title = {{Transcriptional activity generates chromatin motion that drives nuclear blebbing}},
  author = {Kelsey Prince and Nickolas Borowski and Katie Lin and Andy Li and Andrew D. Stephens},
  journal = {Molecular Biology of the Cell},
  year = {2026},
  month = oct,
  doi = {10.1091/mbc.e25-05-0237},
  url = {https://doi.org/10.1091/mbc.e25-05-0237},
  note = {CC BY-NC-SA 4.0},
}
RIS
TY  - JOUR
TI  - Transcriptional activity generates chromatin motion that drives nuclear blebbing
AU  - Kelsey Prince
AU  - Nickolas Borowski
AU  - Katie Lin
AU  - Andy Li
AU  - Andrew D. Stephens
PY  - 2026
DA  - 2026/10/26
JO  - Molecular Biology of the Cell
DO  - 10.1091/mbc.e25-05-0237
UR  - https://doi.org/10.1091/mbc.e25-05-0237
AB  - Abnormal nuclear blebbing is a hallmark of human diseases, including cancers and age-related disorders. Previous work has outlined that nuclear blebbing is due to an imbalance of nuclear strength resisting actin confinement and contraction. Independent of this balance, our recent work revealed that inhibiting RNA polymerase II (RNA Pol II) suppresses nuclear blebbing, but the mechanism remains unknown. Disruption of transcriptional activity through rapid degradation of RNA Pol II via an auxin-inducible degron suppresses nuclear blebbing. To more finely decrease and then restore transcriptional activity, we removed culture media serum and then added it back, respectively. Decreasing transcriptional activity decreases nuclear bleb formation, stability, and rupture, while returning transcriptional activity increases nuclear blebbing. These modulations of transcriptional activity did not alter the nuclear spring constant or actin confinement and contraction. Instead, we find that transcriptional activity regulates chromatin domain motion measured by mean square displacement (MSD) of chromatin domains labeled via transfected Cy3-dNTPs. Increasing chromatin domain motion using an established RAD51 inhibitor B02 resulted in increased nuclear blebbing. Thus, we reveal that transcriptional activity drives nuclear blebbing through chromatin motion.
SN  - 1059-1524
SN  - 1939-4586
ER  -