The nuclear envelope is composed by an outer nuclear membrane and an inner nuclear membrane, which is underlain by the nuclear lamina that provides the nucleus with mechanical strength for maintaining structure and regulates chromatin organization for modulating gene expression and silencing. A layer of heterochromatin is beneath the nuclear lamina, attached by inner nuclear membrane integral proteins such as Lamin B receptor (LBR). LBR is a chimeric protein, having also a sterol reductase activity with which it contributes to cholesterol synthesis. Lukasova et al. showed that when DNA is damaged by ɣ-radiation in cancer cells, LBR is lost causing chromatin structure changes and promoting cellular senescence. Cellular senescence is characterized by terminal cell cycle arrest and the expression and secretion of various growth factors, cytokines, metalloproteinases, etc., collectively known as senescence-associated secretory phenotype (SASP) that cause chronic inflammation and tumor progression when they persist in the tissue. Therefore, it is fundamental to understand the molecular basis for senescence establishment, maintenance and the regulation of SASP. The work of Lukasova et al. contributed to our understanding of cellular senescence establishment and provided the basis that lead to the further discovery that chromatin changes caused by LBR reduction induce an up-regulated expression of SASP factors. LBR dysfunction has relevance in several diseases and possibly in physiological aging. The potential bifunctional role of LBR on cellular senescence establishment, namely its role in chromatin structure together with its enzymatic activity contributing to cholesterol synthesis, provide a new target to develop potential anti-aging therapies.
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July 2020
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Cover Image
Cover Image
3D reconstruction of septin filaments, which orientation is colour coded, bound to liposomes (purple) and obtained by cryo-electron tomography. The polymerization of Shs1 capped protomers is enhanced in the presence of biomimetic membranes. For more information, see the article by Taveneau and colleagues in this issue (pp. 2697–2714). The image was provided by Aurélie Bertin.
Commentary|
July 29 2020
Lamin B receptor: role on chromatin structure, cellular senescence and possibly aging
Susana Castro-Obregón
División de Neurociencias, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México (UNAM), Circuito Exterior SN, Ciudad Universitaria, CDMX 14250, Mexico
Correspondence: Susana Castro-Obregón (scastro@ifc.unam.mx)
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Publisher: Portland Press Ltd
Received:
June 04 2020
Revision Received:
July 09 2020
Accepted:
July 13 2020
Online ISSN: 1470-8728
Print ISSN: 0264-6021
© 2020 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society
2020
Biochem J (2020) 477 (14): 2715–2720.
Article history
Received:
June 04 2020
Revision Received:
July 09 2020
Accepted:
July 13 2020
Connected Content
This is a commentary on:
Loss of lamin B receptor is necessary to induce cellular senescence
Citation
Susana Castro-Obregón; Lamin B receptor: role on chromatin structure, cellular senescence and possibly aging. Biochem J 31 July 2020; 477 (14): 2715–2720. doi: https://doi.org/10.1042/BCJ20200165
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