Journal
NUCLEUS
Volume 3, Issue 5, Pages 411-417Publisher
TAYLOR & FRANCIS INC
DOI: 10.4161/nucl.21674
Keywords
senescence; lamin B1; lamin A; nuclear shape alteration; ataxia telangiectasia; oxidative stress; DNA damage; telomeres; laminopathies
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Funding
- Association pour la Recherche sur le Cancer (ARC)
- Comite des Hauts de Seine de la Ligue Nationale Contre le Cancer
- Division of Life Science (DSV), CEA
- Centre National de Recherche Scientifique (CNRS)
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Progeroid phenotypes are mainly encountered in 2 types of syndromes: in laminopathies, which are characterized by nuclear shape abnormalities due to lamin A alteration, and in DNA damage response defect syndromes. Because lamin A dysregulation leads to DNA damages, it has been proposed that senescence occurs in both types of syndromes through the accumulation of damages. We recently showed that elevated oxidative stress is responsible for lamin B1 accumulation, nuclear shape alteration and senescence in the DDR syndrome, ataxia telangiectasia (A-T). Interestingly, overexpression of lamin B1 in wild type cells is sufficient to induce senescence without the induction of DNA damages. Here, we will discuss the importance of controlling the lamins level in order for maintenance nuclear architecture and we will comment the relationships of lamins with other senescence mechanisms. Finally, we will describe emerging data reporting redox control by lamins, leading us to propose a general mechanism by which reactive oxygen species can induce senescence through lamin dysregulation and NSA.
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