Aging Cell 2015-04-01

Lamin A/C-dependent interaction with 53BP1 promotes cellular responses to DNA damage.

Ian Gibbs-Seymour, Ewa Markiewicz, Simon Bekker-Jensen, Niels Mailand, Christopher J Hutchison

Index: Aging Cell 14(2) , 162-9, (2015)

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Abstract

Lamins A/C have been implicated in DNA damage response pathways. We show that the DNA repair protein 53BP1 is a lamin A/C binding protein. In undamaged human dermal fibroblasts (HDF), 53BP1 is a nucleoskeleton protein. 53BP1 binds to lamins A/C via its Tudor domain, and this is abrogated by DNA damage. Lamins A/C regulate 53BP1 levels and consequently lamin A/C-null HDF display a 53BP1 null-like phenotype. Our data favour a model in which lamins A/C maintain a nucleoplasmic pool of 53BP1 in order to facilitate its rapid recruitment to sites of DNA damage and could explain why an absence of lamin A/C accelerates aging. © 2014 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.

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