Exogenous mechanical cues are transmitted from the extracellular matrix to the nuclear envelope (NE), where mechanical stress on the NE mediates shuttling of transcription factors and other signaling cascades that dictate downstream cellular behavior and fate decisions. To systematically study how nuclear morphology can change across various physiologic microenvironmental contexts, we cultured mesenchymal progenitor cells (MSCs) in engineered 2D and 3D hyaluronic acid hydrogel systems. Across multiple contexts we observed highly 'wrinkled' nuclear envelopes, and subsequently developed a quantitative single-cell imaging metric to better evaluate how wrinkles in the nuclear envelope relate to progenitor cell mechanotransduction. We determined that in soft 2D environments the NE is predominately wrinkled, and that increases in cellular mechanosensing (indicated by cellular spreading, adhesion complex growth, and nuclear localization of YAP/TAZ) occurred only in absence of nuclear envelope wrinkling. Conversely, in 3D hydrogel and tissue contexts, we found NE wrinkling occurred along with increased YAP/TAZ nuclear localization. We further determined that these NE wrinkles in 3D were largely generated by actin impingement, and compared to other nuclear morphometrics, the degree of nuclear wrinkling showed the greatest correlation with nuclear YAP/TAZ localization. These findings suggest that the degree of nuclear envelope wrinkling can predict mechanotransduction state in mesenchymal progenitor cells and highlights the differential mechanisms of NE stress generation operative in 2D and 3D microenvironmental contexts.
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http://dx.doi.org/10.1016/j.biomaterials.2021.120662 | DOI Listing |
Cell Rep
January 2025
Genetics and Epigenetics Program, University of Texas MD Anderson Cancer Center and The University of Texas MD Anderson Cancer Center UTHealth Houston Graduate School of Biomedical Sciences, Houston, TX, USA; Department of Genetics, University of Texas MD Anderson Cancer Center and The University of Texas MD Anderson Cancer Center UTHealth Houston Graduate School of Biomedical Sciences, Houston, TX, USA. Electronic address:
ERK activity oscillates between sustained activation during oocyte formation and transient inactivation during oocyte maturation, fertilization, and early embryogenesis. Consequences of ectopic ERK activity upon oocyte maturation and in early embryogenesis are unknown. We show, in Caenorhabditis elegans, that ectopic ERK activity upon oocyte maturation (metaphase I oocytes) results in embryos with abnormalities in nuclear divisions leading to embryonic death.
View Article and Find Full Text PDFInvest Ophthalmol Vis Sci
January 2025
Department of Physics, Boise State University, Boise, Idaho, United States.
Purpose: To elucidate the mechanical properties of the bovine lens cortical membrane (CM), the nuclear membrane (NM) containing cholesterol bilayer domains (CBDs), and whole bovine lenses.
Methods: The total lipids (lipids plus cholesterol) from the cortex and nucleus of a single bovine lens were isolated using the monophasic methanol extraction method. Supported CMs and NMs were prepared from total lipids extracted from the cortex and nucleus, respectively, using a rapid solvent exchange method and probe-tip sonication, followed by the fusion of unilamellar vesicles on a flat, freshly cleaved mica surface.
Nucleus
December 2025
Center for Translational Medicine, Department of Medicine, Thomas Jefferson University, Philadelphia, PA, USA.
Over the past 25 years, nuclear envelope (NE) perturbations have been reported in various experimental models with mutations in the gene. Although the hypothesis that NE perturbations from mutations are a fundamental feature of striated muscle damage has garnered wide acceptance, the molecular sequalae provoked by the NE damage and how they underlie disease pathogenesis such as cardiomyopathy ( cardiomyopathy) remain poorly understood. We recently shed light on one such consequence, by employing a cardiomyocyte-specific deletion in the adult heart.
View Article and Find Full Text PDFMol Biol Cell
January 2025
Department of Chemistry and Biochemistry, University of California, Los Angeles, Los Angeles, CA 90095, USA.
SPOP is a Cul3 substrate adaptor responsible for the degradation of many proteins related to cell growth and proliferation. Because mutation or misregulation of SPOP drives cancer progression, understanding the suite of SPOP substrates is important to understanding the regulation of cell proliferation. Here, we identify Nup153, a component of the nuclear basket of the nuclear pore complex, as a novel substrate of SPOP.
View Article and Find Full Text PDFNat Cell Biol
January 2025
CNRS UMR144 - UMR3664, Institut Curie, Sorbonne Université, PSL Research University, Paris, France.
Errors during cell division lead to aneuploidy, which is associated with genomic instability and cell transformation. In response to aneuploidy, cells activate the tumour suppressor p53 to elicit a surveillance mechanism that halts proliferation and promotes senescence. The molecular sensors that trigger this checkpoint are unclear.
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