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JCI table of contents: Sept. 4, 2007
Date:9/4/2007

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PHYSIOLOGY: ATM banks two new functions

Ataxia-telangiectasia (A-T) is a fatal childhood disorder caused by mutations in the gene encoding ATM. ATM coordinates the cellular response to DNA damage and although many of the symptoms of A-T can be explained by the loss of this function, not all can. In a new study, Gerald Shadel and colleagues from Yale University have identified two additional functions for ATM that might contribute to the pathology of A-T.

Analysis of tissues from patients with A-T and mice lacking ATM indicated that ATM regulates the level of expression and/or stability of ribonucleotide reductase (RR), the enzyme that mediates the rate-limiting step in the de novo synthesis of deoxyribonucleoside triphosphates, the building blocks of RNA. ATM and RR were also required to maintain normal levels of mitochondrial DNA, which is important for maintaining normal functioning of the mitochondria. In addition to providing insight into the molecular mechanisms responsible for the symptoms of A-T, the authors suggested that this study indicates that inherited mitochondrial DNA–depletion syndromes in humans (a fatal class of diseases) might be caused by mutations in the genes encoding the RR subunits.

TITLE: Ataxia-telangiectasia mutated kinase regulates ribonucleotide reductase and mitochondrial homeostasis

AUTHOR CONTACT:

Gerald S. Shadel
Yale University School of Medicine, New Haven, Connecticut, USA.
Phone: (203) 785-2475; Fax: (203) 785-2628; E-mail: gerald.shadel@yale.edu.

Jacqueline E. Weaver
Yale University Office of Public Affairs, New Haven, Connecticut, USA.
Phone: (203) 432-8555; Fax: (203) 432-1323; E-mail: jacqueline.weaver@yale.edu

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Contact: Karen Honey
press_releases@the-jci.org
215-573-1850
Journal of Clinical Investigation
Source:Eurekalert

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