Relevant bibliographies by topics / DNA damage: Cell migration Nuclear envelope

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Academic literature on the topic 'DNA damage: Cell migration Nuclear envelope'

Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "DNA damage: Cell migration Nuclear envelope"

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Raab, M., M. Gentili, H. de Belly, H. R. Thiam, P. Vargas, A. J. Jimenez, F. Lautenschlaeger, et al. "ESCRT III repairs nuclear envelope ruptures during cell migration to limit DNA damage and cell death." Science 352, no. 6283 (March 24, 2016): 359–62. http://dx.doi.org/10.1126/science.aad7611.

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Pfeifer, Charlotte R., Manasvita Vashisth, Yuntao Xia, and Dennis E. Discher. "Nuclear failure, DNA damage, and cell cycle disruption after migration through small pores: a brief review." Essays in Biochemistry 63, no. 5 (July 31, 2019): 569–77. http://dx.doi.org/10.1042/ebc20190007.

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Abstract In many contexts of development, regeneration, or disease such as cancer, a cell squeezes through a dense tissue or a basement membrane, constricting its nucleus. Here, we describe how the severity of nuclear deformation depends on a nucleus’ mechanical properties that are mostly determined by the density of chromatin and by the nuclear lamina. We explain how constriction-induced nuclear deformation affects nuclear contents by causing (i) local density changes in chromatin and (ii) rupture of the nuclear lamina and envelope. Both processes mislocalize diffusible nuclear factors including key DNA repair and regulatory proteins. Importantly, these effects of constricted migration are accompanied by excess DNA damage, marked by phosphorylated histone γH2AX in fixed cells. Rupture has a number of downstream consequences that include a delayed cell cycle—consistent with a damage checkpoint—and modulation of differentiation, both of which are expected to affect migration-dependent processes ranging from wound healing to tumorigenic invasion.
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Irianto, Jerome, Charlotte R. Pfeifer, Rachel R. Bennett, Yuntao Xia, Irena L. Ivanovska, Andrea J. Liu, Roger A. Greenberg, and Dennis E. Discher. "Nuclear constriction segregates mobile nuclear proteins away from chromatin." Molecular Biology of the Cell 27, no. 25 (December 15, 2016): 4011–20. http://dx.doi.org/10.1091/mbc.e16-06-0428.

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As a cell squeezes its nucleus through adjacent tissue, penetrates a basement membrane, or enters a small blood capillary, chromatin density and nuclear factors could in principle be physically perturbed. Here, in cancer cell migration through rigid micropores and in passive pulling into micropipettes, local compaction of chromatin is observed coincident with depletion of mobile factors. Heterochromatin/euchromatin was previously estimated from molecular mobility measurements to occupy a volume fraction f of roughly two-thirds of the nuclear volume, but based on the relative intensity of DNA and histones in several cancer cell lines drawn into narrow constrictions, f can easily increase locally to nearly 100%. By contrast, mobile proteins in the nucleus, including a dozen that function as DNA repair proteins (e.g., BRCA1, 53BP1) or nucleases (e.g., Cas9, FokI), are depleted within the constriction, approaching 0%. Such losses—compounded by the occasional rupture of the nuclear envelope—can have important functional consequences. Studies of a nuclease that targets a locus in chromosome-1 indeed show that constricted migration delays DNA damage.
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Howell, D. M., and E. Martz. "Nuclear disintegration induced by cytotoxic T lymphocytes. Evidence against damage to the nuclear envelope of the target cell." Journal of Immunology 140, no. 3 (February 1, 1988): 689–92. http://dx.doi.org/10.4049/jimmunol.140.3.689.

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Abstract CTL and NK cells induce nuclear disintegration in their target cells. This phenomenon, which is seen as extensive fragmentation and solubilization of target cell DNA, is not seen with most other means of inducing cytolysis, including antibody- and complement-mediated cytolysis. We have previously shown that the degree of DNA solubilization is dependent upon the nature of the target cell. We here investigate the possibility that CTL induce, in all targets, damage to the nuclear envelope, which in turn leads to nuclear disintegration in only some of them. We reasoned that damage to the nuclear envelope would render nuclear DNA more accessible to exogenous DNase. Therefore, we determined the susceptibility of target DNA to exogenous DNase I after cytolysis by various means. We found no difference in DNA susceptibility for cells lysed by CTL vs methods (such as complement-mediated lysis or nonionic detergent) incapable of inducing nuclear disintegration. As a positive control, freezing and thawing dramatically enhanced susceptibility of the DNA. In conclusion, we found no evidence that the nuclear envelope is damaged by CTL in target cell types (or in the subpopulation of nuclei) that do not undergo nuclear disintegration.
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Smith, Lucas R., Jerome Irianto, Yuntao Xia, Charlotte R. Pfeifer, and Dennis E. Discher. "Constricted migration modulates stem cell differentiation." Molecular Biology of the Cell 30, no. 16 (July 22, 2019): 1985–99. http://dx.doi.org/10.1091/mbc.e19-02-0090.

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Tissue regeneration at an injured site depends on proliferation, migration, and differentiation of resident stem or progenitor cells, but solid tissues are often sufficiently dense and constricting that nuclei are highly stressed by migration. In this study, constricted migration of myoblastic cell types and mesenchymal stem cells (MSCs) increases nuclear rupture, increases DNA damage, and modulates differentiation. Fewer myoblasts fuse into regenerating muscle in vivo after constricted migration in vitro, and myodifferentiation in vitro is likewise suppressed. Myosin II inhibition rescues rupture and DNA damage, implicating nuclear forces, while mitosis and the cell cycle are suppressed by constricted migration, consistent with a checkpoint. Although perturbed proliferation fails to explain defective differentiation, nuclear rupture mislocalizes differentiation-relevant MyoD and KU80 (a DNA repair factor), with nuclear entry of the DNA-binding factor cGAS. Human MSCs exhibit similar damage, but osteogenesis increases—which is relevant to bone and to calcified fibrotic tissues, including diseased muscle. Tissue repair can thus be modulated up or down by the curvature of pores through which stem cells squeeze.
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Pfeifer, Charlotte R., Yuntao Xia, Kuangzheng Zhu, Dazhen Liu, Jerome Irianto, Victor M. Morales García, Leeza M. Santiago Millán, et al. "Constricted migration increases DNA damage and independently represses cell cycle." Molecular Biology of the Cell 29, no. 16 (August 8, 2018): 1948–62. http://dx.doi.org/10.1091/mbc.e18-02-0079.

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Cell migration through dense tissues or small capillaries can elongate the nucleus and even damage it, and any impact on cell cycle has the potential to affect various processes including carcinogenesis. Here, nuclear rupture and DNA damage increase with constricted migration in different phases of cell cycle—which we show is partially repressed. We study several cancer lines that are contact inhibited or not and that exhibit diverse frequencies of nuclear lamina rupture after migration through small pores. DNA repair factors invariably mislocalize after migration, and an excess of DNA damage is evident as pan-­nucleoplasmic foci of phosphoactivated ATM and γH2AX. Foci counts are suppressed in late cell cycle as expected of mitotic checkpoints, and migration of contact-inhibited cells through large pores into sparse microenvironments leads also as expected to cell-cycle reentry and no effect on a basal level of damage foci. Constricting pores delay such reentry while excess foci occur independent of cell-cycle phase. Knockdown of repair factors increases DNA damage independent of cell cycle, consistent with effects of constricted migration. Because such migration causes DNA damage and impedes proliferation, it illustrates a cancer cell fate choice of “go or grow.”
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Patteson, Alison E., Amir Vahabikashi, Katarzyna Pogoda, Stephen A. Adam, Kalpana Mandal, Mark Kittisopikul, Suganya Sivagurunathan, Anne Goldman, Robert D. Goldman, and Paul A. Janmey. "Vimentin protects cells against nuclear rupture and DNA damage during migration." Journal of Cell Biology 218, no. 12 (November 1, 2019): 4079–92. http://dx.doi.org/10.1083/jcb.201902046.

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Mammalian cells frequently migrate through tight spaces during normal embryogenesis, wound healing, diapedesis, or in pathological situations such as metastasis. Nuclear size and shape are important factors in regulating the mechanical properties of cells during their migration through such tight spaces. At the onset of migratory behavior, cells often initiate the expression of vimentin, an intermediate filament protein that polymerizes into networks extending from a juxtanuclear cage to the cell periphery. However, the role of vimentin intermediate filaments (VIFs) in regulating nuclear shape and mechanics remains unknown. Here, we use wild-type and vimentin-null mouse embryonic fibroblasts to show that VIFs regulate nuclear shape and perinuclear stiffness, cell motility in 3D, and the ability of cells to resist large deformations. These changes increase nuclear rupture and activation of DNA damage repair mechanisms, which are rescued by exogenous reexpression of vimentin. Our findings show that VIFs provide mechanical support to protect the nucleus and genome during migration.
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Xia, Yuntao, Charlotte R. Pfeifer, Kuangzheng Zhu, Jerome Irianto, Dazhen Liu, Kalia Pannell, Emily J. Chen, et al. "Rescue of DNA damage after constricted migration reveals a mechano-regulated threshold for cell cycle." Journal of Cell Biology 218, no. 8 (June 25, 2019): 2545–63. http://dx.doi.org/10.1083/jcb.201811100.

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Migration through 3D constrictions can cause nuclear rupture and mislocalization of nuclear proteins, but damage to DNA remains uncertain, as does any effect on cell cycle. Here, myosin II inhibition rescues rupture and partially rescues the DNA damage marker γH2AX, but an apparent block in cell cycle appears unaffected. Co-overexpression of multiple DNA repair factors or antioxidant inhibition of break formation also exert partial effects, independently of rupture. Combined treatments completely rescue cell cycle suppression by DNA damage, revealing a sigmoidal dependence of cell cycle on excess DNA damage. Migration through custom-etched pores yields the same damage threshold, with ∼4-µm pores causing intermediate levels of both damage and cell cycle suppression. High curvature imposed rapidly by pores or probes or else by small micronuclei consistently associates nuclear rupture with dilution of stiff lamin-B filaments, loss of repair factors, and entry from cytoplasm of chromatin-binding cGAS (cyclic GMP-AMP synthase). The cell cycle block caused by constricted migration is nonetheless reversible, with a potential for DNA misrepair and genome variation.
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Houthaeve, Gaëlle, Joke Robijns, Kevin Braeckmans, and Winnok H. De Vos. "Bypassing Border Control: Nuclear Envelope Rupture in Disease." Physiology 33, no. 1 (January 1, 2018): 39–49. http://dx.doi.org/10.1152/physiol.00029.2017.

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Recent observations in laminopathy patient cells and cancer cells have revealed that the nuclear envelope (NE) can transiently rupture during interphase. NE rupture leads to an uncoordinated exchange of nuclear and cytoplasmic material, thereby deregulating cellular homeostasis. Moreover, concurrently inflicted DNA damage could prime rupture-prone cells for genome instability. Thus, NE rupture may represent a novel pathogenic mechanism that has far-reaching consequences for cell and organism physiology.
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Kirchenbauer, Marisa, and Dimitris Liakopoulos. "An auxiliary, membrane-based mechanism for nuclear migration in budding yeast." Molecular Biology of the Cell 24, no. 9 (May 2013): 1434–43. http://dx.doi.org/10.1091/mbc.e12-08-0602.

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How nuclear shape correlates with nuclear movements during the cell cycle is poorly understood. We investigated changes in nuclear morphology during nuclear migration in budding yeast. In preanaphase cells, nuclear protrusions (nucleopodia [NP]) extend into the bud, preceding insertion of chromosomes into the bud neck. Surprisingly, formation of nucleopodia did not depend on the established nuclear migration pathways. We show that generation and maintenance of NP requires nuclear membrane expansion, actin, and the exocyst complex. Exocyst mutations cause nuclear positioning defects and display genetic interactions with mutations that deactivate astral microtubule-dependent nuclear migration. Cells that cannot perform DNA replication also fail to form nucleopodia. We propose that nuclear membrane expansion, DNA replication, and exocyst-dependent anchoring of the nuclear envelope to the bud affect nuclear morphology and facilitate correct positioning of nucleus and chromosomes relative to the cleavage apparatus.
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Dissertations / Theses on the topic "DNA damage: Cell migration Nuclear envelope"

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KIDIYOOR, GURURAJ RAO. "ATR MEDIATED REGULATION OF CELLULAR AND NUCLEAR PLASTICITY." Doctoral thesis, Università degli Studi di Milano, 2018. http://hdl.handle.net/2434/561090.

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Protein kinase ATR (Ataxia Telangiectasia and Rad3-related) is a key regulator of genomic integrity. In addition to its vital, well-understood role in maintaining replication fork stability, ATR is also involved in mediating mechanical stress response at the nuclear envelope preventing potential threats to the genome. Our data from sub-cellular distribution and interactome analysis of ATR suggests that ATR contributes to several cellular processes in multiple organelles such as mitochondria, actin cytoskeleton, Golgi and nuclear envelope. At the nuclear envelope ATR is present on both inner and outer nuclear membranes, on the nuclear pores and bound to perinuclear chromatin and to perinuclear actin fibers. In this study we show that ATR regulates nuclear membrane integrity by maintaining nuclear morphology and optimal membrane tension, by counteracting mechanical force imbalances at the NE and by coordinating nuclear events with nuclear and cell migration. We report a novel role of ATR in preventing and protecting nuclear envelope damage and DNA damage caused by mechanical constrains acting on the nucleus. Further we show that by maintaining nuclear envelope integrity ATR facilitates cell migration on 2D surfaces and by regulating nuclear membrane components and by limiting nuclear envelope damage it aids cell survival during confined 3D migrations. Loss of ATR dampens neuronal migration during development and cancer cells lacking ATR are inefficient in extravasation, do not survive circulation and fail to successfully metastasize into the host environment. Therefore, by promoting cell survival in altering mechanical microenvironment and during metastasis and invasion, ATR assists tumor development, suggesting a dual role for this kinase in tumorigenisis
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Book chapters on the topic "DNA damage: Cell migration Nuclear envelope"

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Koleckova, Marketa, Katherine Vomackova, and Zdenek Kolar. "Molecular Prognostic and Predictive Markers in Triple - Negative Breast Cancer." In Breast Cancer [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97282.

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Triple-negative breast cancer (TNBC) is defined as a molecular subtype of breast cancer that lacks expression of hormone receptors (oestrogen and progesterone receptor) and HER2/neu/ErbB2 protein. It accounts for 15–20% of all invasive breast cancers. The occurrence of TNBC is often associated with younger age at the time of diagnosis and pre-menopausal status, early onset of menarche, higher body mass index (BMI) in the pre-menopausal period, race and ethnicity (African, Hispanic) and the presence of germline mutation in the BRCA1/2 genes or somatic mutation in the TP53 or PTEN genes. TNBCs are specific in its aggressive biological behaviour, shorter interval to disease progression and more frequent relapse within five years (19 to 40 months). The most of TNBCs are represented by high-grade invasive carcinomas of no special type (NST) with high proliferation index measured by Ki-67 nuclear expression, followed by metaplastic carcinomas, secretory carcinomas, and adenoid cystic carcinomas. Genetical and morphological heterogeneity inside TNBC is responsible for the higher frequency of primary and secondary resistance to systemic therapy. The scope of this chapter is to summarise the potential therapeutic agents involved in regulation of cell proliferation, migration, angiogenesis, apoptosis, gene expression and DNA damage or immune response. The insight into this issue is essential for the setting of the optimal chemotherapy regimen and targeted therapeutic strategy.
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