@article{12880,
  abstract     = {Peripheral heterochromatin positioning depends on nuclear envelope associated proteins and repressive histone modifications. Here we show that overexpression (OE) of Lamin B1 (LmnB1) leads to the redistribution of peripheral heterochromatin into heterochromatic foci within the nucleoplasm. These changes represent a perturbation of heterochromatin binding at the nuclear periphery (NP) through a mechanism independent from altering other heterochromatin anchors or histone post-translational modifications. We further show that LmnB1 OE alters gene expression. These changes do not correlate with different levels of H3K9me3, but a significant number of the misregulated genes were likely mislocalized away from the NP upon LmnB1 OE. We also observed an enrichment of developmental processes amongst the upregulated genes. ~74% of these genes were normally repressed in our cell type, suggesting that LmnB1 OE promotes gene de-repression. This demonstrates a broader consequence of LmnB1 OE on cell fate, and highlights the importance of maintaining proper levels of LmnB1.},
  author       = {Kaneshiro, Jeanae M. and Capitanio, Juliana S. and Hetzer, Martin W},
  issn         = {1949-1042},
  journal      = {Nucleus},
  number       = {1},
  publisher    = {Taylor & Francis},
  title        = {{Lamin B1 overexpression alters chromatin organization and gene expression}},
  doi          = {10.1080/19491034.2023.2202548},
  volume       = {14},
  year         = {2023},
}

@article{11091,
  abstract     = {Neoplastic cells are often characterized by specific morphological abnormalities of the nuclear envelope (NE), which have been used for cancer diagnosis for more than a century. The NE is a double phospholipid bilayer that encapsulates the nuclear genome, regulates all nuclear trafficking of RNAs and proteins and prevents the passive diffusion of macromolecules between the nucleoplasm and the cytoplasm. Whether there is a consequence to the proper functioning of the cell and loss of structural integrity of the nucleus remains unclear. Using live cell imaging, we characterize a phenomenon wherein nuclei of several proliferating human cancer cell lines become temporarily ruptured during interphase. Strikingly, NE rupturing was associated with the mislocalization of nucleoplasmic and cytoplasmic proteins and, in the most extreme cases, the entrapment of cytoplasmic organelles in the nuclear interior. In addition, we observed the formation of micronuclei-like structures during interphase and the movement of chromatin out of the nuclear space. The frequency of these NE rupturing events was higher in cells in which the nuclear lamina, a network of intermediate filaments providing mechanical support to the NE, was not properly formed. Our data uncover the existence of a NE instability that has the potential to change the genomic landscape of cancer cells.},
  author       = {Vargas, Jesse D. and Hatch, Emily M. and Anderson, Daniel J. and HETZER, Martin W},
  issn         = {1949-1042},
  journal      = {Nucleus},
  keywords     = {Cell Biology},
  number       = {1},
  pages        = {88--100},
  publisher    = {Taylor & Francis},
  title        = {{Transient nuclear envelope rupturing during interphase in human cancer cells}},
  doi          = {10.4161/nucl.18954},
  volume       = {3},
  year         = {2012},
}