Lessons from senescence: chromatin maintenance in non-proliferating cells

Rai, T.S. and Adams, P.D. (2012) Lessons from senescence: chromatin maintenance in non-proliferating cells. Biochimica et Biophysica Acta: Gene Regulatory Mechanisms, 1819(3-4), pp. 322-331. (doi: 10.1016/j.bbagrm.2011.07.014) (PMID:21839870) (PMCID:PMC3895594)

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Cellular senescence is an irreversible proliferation arrest, thought to contribute to tumor suppression, proper wound healing and, perhaps, tissue and organismal aging. Two classical tumor suppressors, p53 and pRB, control cell cycle arrest associated with senescence. Profound molecular changes occur in cells undergoing senescence. At the level of chromatin, for example, senescence associated heterochromatic foci (SAHF) form in some cell types. Chromatin is inherently dynamic and likely needs to be actively maintained to achieve a stable cell phenotype. In proliferating cells chromatin is maintained in conjunction with DNA replication, but how non-proliferating cells maintain chromatin structure is poorly understood. Some histone variants, such as H3.3 and macroH2A increase as cells undergo senescence, suggesting histone variants and their associated chaperones could be important in chromatin structure maintenance in senescent cells. Here, we discuss options available for senescent cells to maintain chromatin structure and the relative contribution of histone variants and chaperones in this process. This article is part of a Special Issue entitled: Histone chaperones and chromatin assembly.

Item Type:Articles
Glasgow Author(s) Enlighten ID:Rai, Dr Taranjit and Adams, Professor Peter
Authors: Rai, T.S., and Adams, P.D.
College/School:College of Medical Veterinary and Life Sciences > School of Cancer Sciences
Journal Name:Biochimica et Biophysica Acta: Gene Regulatory Mechanisms
ISSN (Online):1876-4320
Published Online:03 August 2011

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Project CodeAward NoProject NamePrincipal InvestigatorFunder's NameFunder RefLead Dept
495301Tumor progression - its antagonistic regulation by Wnt-signalling and oncogene-induced senescence.Peter AdamsCancer Research UK (CAN-RES-UK)C10652/A10250Institute of Cancer Sciences