Journal ArticleDOI
Mechanisms and functions of nuclear envelope remodelling
Rosemarie Ungricht,Ulrike Kutay +1 more
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The nuclear envelope is shown to be a dynamic and highly adaptable boundary that changes composition during differentiation, deforms in response to mechanical challenges, can be repaired upon rupture and even rapidly disassembles and reforms during open mitosis.Abstract:
As a compartment border, the nuclear envelope (NE) needs to serve as both a protective membrane shell for the genome and a versatile communication interface between the nucleus and the cytoplasm. Despite its important structural role in sheltering the genome, the NE is a dynamic and highly adaptable boundary that changes composition during differentiation, deforms in response to mechanical challenges, can be repaired upon rupture and even rapidly disassembles and reforms during open mitosis. NE remodelling is fundamentally involved in cell growth, division and differentiation, and if perturbed can lead to devastating diseases such as muscular dystrophies or premature ageing.read more
Citations
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Journal ArticleDOI
LINCking the Nuclear Envelope to Sperm Architecture.
TL;DR: The LINC (linker of nucleoskeleton and cytoskeleton) complex as mentioned in this paper is a nuclear envelope-bridge structure involved in the connection of the nucleos skeleton to the cytos skeleton, governing mechanotransduction, and is involved in several functions fundamental to the correct development of sperm cells such as head formation and head to tail connection.
Journal ArticleDOI
Nuclear Envelope Alterations in Myotonic Dystrophy Type 1 Patient-Derived Fibroblasts
Diana Viegas,Cátia D. Pereira,Filipa Martins,Tiago Mateus,Odete A. B. da Cruz e Silva,Maria Teresa Herdeiro,Sandra Rebelo +6 more
TL;DR: Evidence is reinforced that NE dysfunction is a highly relevant pathological characteristic observed in DM1 by demonstrating that DM1 patient-derived fibroblasts exhibited altered intracellular protein levels and subcellular distribution of relevant NE proteins in these cell lines.
Posted ContentDOI
Dynein Pulling Forces On Ruptured Nuclei Counteract Lamin-Mediated Nuclear Envelope Repair Mechanisms In Vivo
Lauren Penfield,Brian Wysolmerski,Reza Farhadifar,Michael A. Q. Martinez,Ronald Biggs,Hai-Yin Wu,Michael Mauro,Curtis Broberg,Daniel J. Needleman,Shirin Bahmanyar +9 more
TL;DR: It is demonstrated that lamin controls the duration of NE ruptures by opposing dynein forces on ruptured nuclei to allow reestablishment of the NE permeability barrier and subsequent restoration of NE rupture sites.
Journal ArticleDOI
Reprogramming tumor-associated macrophages as a unique approach to target tumor immunotherapy
Safir Ullah Khan,Munir Ullah Khan,Ibrar Khan,Muhammad Imran Khan,Simona Bungau,Syed Shams ul Hassan +5 more
TL;DR: TAMs in particular are the most common kind of leucocyte in many malignancies and play a crucial role in establishing a favorable microenvironment for tumor cells as discussed by the authors .
Journal ArticleDOI
Spindle Dynamics during Meiotic Development of the Fungus Podospora anserina Requires the Endoplasmic Reticulum-Shaping Protein RTN1.
Antonio de Jesús López-Fuentes,Karime Naid Nachón-Garduño,Fernando Suaste-Olmos,Ariadna Mendieta-Romero,Leonardo Peraza-Reyes +4 more
TL;DR: In this article, the function of reticulon (RTN1) and Yop1 proteins (YOP1 and YOP2) of the model fungus Podospora anserina and their contribution to sexual development was analyzed.
References
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Journal ArticleDOI
Massive Genomic Rearrangement Acquired in a Single Catastrophic Event during Cancer Development
Philip J. Stephens,Christopher Greenman,Beiyuan Fu,Fengtang Yang,Graham R. Bignell,Laura Mudie,Erin Pleasance,King Wai Lau,David Beare,Lucy Stebbings,Stuart McLaren,Meng-Lay Lin,David J. McBride,Ignacio Varela,Serena Nik-Zainal,Catherine Leroy,Mingming Jia,Andrew Menzies,Adam Butler,Jon W. Teague,Michael A. Quail,John Burton,Harold Swerdlow,Nigel P. Carter,Laura Morsberger,Christine A. Iacobuzio-Donahue,George A. Follows,Anthony R. Green,Adrienne M. Flanagan,Adrienne M. Flanagan,Michael R. Stratton,P. Andrew Futreal,Peter J. Campbell,Peter J. Campbell +33 more
TL;DR: It is found that one, or indeed more than one, cancer-causing lesion can emerge out of the genomic crisis, which has important implications for the origins of genomic remodeling and temporal emergence of cancer.
Journal ArticleDOI
Recurrent de novo point mutations in lamin A cause Hutchinson-Gilford progeria syndrome
Maria Eriksson,W. Ted Brown,Leslie B. Gordon,Leslie B. Gordon,Michael W. Glynn,Joel Singer,Laura J. Scott,Michael R. Erdos,Christiane M. Robbins,Tracy Moses,Peter Berglund,Amalia Dutra,Evgenia Pak,Sandra G. Durkin,Antonei B. Csoka,Michael Boehnke,Thomas W. Glover,Francis S. Collins +17 more
TL;DR: Evidence of mutations in lamin A (LMNA) as the cause of Hutchinson–Gilford progeria syndrome is presented, and the discovery of the molecular basis of this disease may shed light on the general phenomenon of human ageing.
Journal ArticleDOI
Domain organization of human chromosomes revealed by mapping of nuclear lamina interactions
Lars Guelen,Ludo Pagie,Emilie Brasset,Wouter Meuleman,Wouter Meuleman,Marius B. Faza,Wendy Talhout,Bert H.J. Eussen,Annelies de Klein,Lodewyk F. A. Wessels,Lodewyk F. A. Wessels,Wouter de Laat,Bas van Steensel +12 more
TL;DR: A high-resolution map of the interaction sites of the entire genome with NL components in human fibroblasts is constructed and demonstrates that the human genome is divided into large, discrete domains that are units of chromosome organization within the nucleus.
Journal ArticleDOI
Nuclear lamin-A Scales With Tissue Stiffness and Enhances Matrix-Directed Differentiation
Joe Swift,Irena L. Ivanovska,Amnon Buxboim,Takamasa Harada,P.C. Dave P. Dingal,Joel Pinter,J. David Pajerowski,Kyle R. Spinler,Jae-Won Shin,Manorama Tewari,Florian Rehfeldt,David W. Speicher,Dennis E. Discher,Dennis E. Discher +13 more
TL;DR: In this article, proteomics analyses revealed that levels of the nucleoskeletal protein lamin-A scaled with tissue elasticity, as did levels of collagens in the extracellular matrix that determine E.
Journal ArticleDOI
Genomic Instability and Aging-like Phenotype in the Absence of Mammalian SIRT6
Raul Mostoslavsky,Katrin F. Chua,Katrin F. Chua,David B. Lombard,Wendy W. Pang,Miriam R. Fischer,Lionel Gellon,Pingfang Liu,Gustavo Mostoslavsky,Sonia Franco,Michael M. Murphy,Kevin D. Mills,Parin Patel,Joyce T. Hsu,Andrew L. Hong,Ethan Ford,Hwei Ling Cheng,Caitlin Kennedy,Nomeli P. Nunez,Nomeli P. Nunez,Roderick T. Bronson,David Frendewey,Wojtek Auerbach,David M. Valenzuela,Margaret Karow,Michael O. Hottiger,Stephen D. Hursting,J. Carl Barrett,J. Carl Barrett,Leonard Guarente,Richard C. Mulligan,Bruce Demple,George D. Yancopoulos,Frederick W. Alt +33 more
TL;DR: It is demonstrated that SIRT6 is a nuclear, chromatin-associated protein that promotes resistance to DNA damage and suppresses genomic instability in mouse cells, in association with a role in base excision repair (BER).