Genetics. Published Articles Ahead of Print: August 20, 2008, Copyright © 2008
doi:10.1534/genetics.108.090704


A more recent version of this article appeared on September 1, 2008.


NOTE

Maintenance of mitochondrial DNA by the C. elegans ATR checkpoint protein ATL-1

1 Tohoku University, Graduate School of Life Sciences

* To whom correspondence should be addressed. E-mail: ahigashi{at}ige.tohoku.ac.jp.

Submitted on April 28, 2008
Revised on May 26, 2008
Accepted on 19 June 2008


Abstract

Here we show that inactivation of the ATR-related kinase ATL-1 results in a significant reduction in mitochondrial DNA (mtDNA) copy numbers in C. elegans. Although ribonucleotide reductase (RNR) expression and the ATP/dATP ratio remained unaltered in atl-1 deletion mutants, inhibition of RNR by RNAi or hydroxyurea treatment caused further reductions in mtDNA copy number. These results suggest that ATL-1 functions to maintain mtDNA independently of RNR.

Key Words: ataxia-telangiectasia, checkpoint control, mitochondrial DNA, replication, ribonucleotide reductase