Increased cell-to-cell variation in gene expression in ageing mouse heart

Rumana Bahar, Claudia H. Hartmann, Karl A. Rodriguez, Ashley D. Denny, Rita A. Busuttil, Martijn E. T. Dollé, R. Brent Calder, Gary B. Chisholm, Brad H. Pollock, Christoph A. Klein and Jan Vijg ()
Additional contact information
Rumana Bahar: Buck Institute for Age Research
Claudia H. Hartmann: Institut für Immunologie, Ludwig-Maximilians Universität
Karl A. Rodriguez: University of Texas Health Science Center
Ashley D. Denny: University of Texas Health Science Center
Rita A. Busuttil: Buck Institute for Age Research
Martijn E. T. Dollé: National Institute of Public Health and the Environment
R. Brent Calder: Buck Institute for Age Research
Gary B. Chisholm: University of Texas Health Science Center
Brad H. Pollock: University of Texas Health Science Center
Christoph A. Klein: Institut für Immunologie, Ludwig-Maximilians Universität
Jan Vijg: Buck Institute for Age Research

Nature, 2006, vol. 441, issue 7096, 1011-1014

Abstract: Old at heart Changes in the control of gene expression due to random damage to the genome have long been considered a possible cause of ageing. A study of heart tissues in young (aged 6 months) and old mice (aged 27 months) provides important data to support that theory. It shows for the first time that there is intrinsic variability in gene expression in cells freshly isolated from mouse heart, and that variability increases with age. Treatment with genotoxic chemicals mimics the effect of ageing. The results point to deregulation of gene expression by chance events as a general mechanism of ageing-related cellular degeneration and death.

Date: 2006
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DOI: 10.1038/nature04844

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