53BP1 Contributes to a Robust Genomic Stability in Human Fibroblasts

Overview

Journal Aging (Albany NY)

Specialty Geriatrics

Date 2011 Sep 21

PMID 21931182

Citations 16

Authors

Lauren S Fink

Michaela Roell

Emanuela Caiazza

Chad Lerner

Thomas Stamato

Silvana Hrelia

Antonello Lorenzini

Christian Sell

Affiliations

Soon will be listed here.

Abstract

Faithful repair of damaged DNA is a crucial process in maintaining cell viability and function. A multitude of factors and pathways guides this process and includes repair proteins and cell cycle checkpoint factors. Differences in the maintenance of genomic processes are one feature that may contribute to species-specific differences in lifespan. We predicted that 53BP1, a key transducer of the DNA damage response and cell cycle checkpoint control, is highly involved in maintaining genomic stability and may function differently in cells from different species. We demonstrate a difference in the levels and recruitment of 53BP1 in mouse and human cells following DNA damage. In addition, we show that unresolved DNA damage persists more in mouse cells than in human cells, as evidenced by increased numbers of micronuclei. The difference in micronuclei seems to be related to the levels of 53BP1 present in cells. Finally, we present evidence that unresolved DNA damage correlates with species lifespan. Taken together, these studies suggest a link between recruitment of 53BP1, resolution of DNA damage, and increased species lifespan.

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