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Molecular and Cellular Biology, January 2005, p. 294-302, Vol. 25, No. 1
0270-7306/05/$08.00+0     doi:10.1128/MCB.25.1.294-302.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Generation and Characterization of Endonuclease G Null Mice{dagger}

Ryan A. Irvine,1 Noritaka Adachi,1 Darryl K. Shibata,1 Geoffrey D. Cassell,1 Kefei Yu,1 Zarir E. Karanjawala,1 Chih-Lin Hsieh,2 and Michael R. Lieber1*

Departments of Pathology, of Biochemistry & Molecular Biology, of Molecular Microbiology & Immunology, and of Biological Sciences,1 Departments of Urology and of Biochemistry & Molecular Biology, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, California2

Received 19 August 2004/ Returned for modification 24 September 2004/ Accepted 10 October 2004

Endonuclease G (endo G) is one of the most abundant nucleases in eukaryotic cells. It is encoded in the nucleus and imported to the mitochondrial intermembrane space. This nuclease is active on single- and double-stranded DNA. We genetically disrupted the endo G gene in mice without disturbing a conserved, overlapping gene of unknown function that is oriented tail to tail with the endo G gene. In these mice, the production of endo G protein is not detected, and the disruption abolishes the nuclease activity of endo G. The absence of endo G has no effect on mitochondrial DNA copy number, structure, or mutation rate over the first five generations. There is also no obvious effect on nuclear DNA degradation in standard apoptosis assays. The endo G null mice are viable and show no age-related or generational abnormalities anatomically or histologically. We infer that this highly conserved protein has no mitochondrial or apoptosis function that can discerned by the assays described here and that it may have a function yet to be determined. The early embryonic lethality of endo G null mice recently reported by others may be due to the disruption of the gene that overlaps the endo G gene.

* Corresponding author. Mailing address: Norris Comprehensive Cancer Center, Rm. 5428, Keck School of Medicine, University of Southern California, 1441 Eastlake Ave., MC9176, Los Angeles, CA 90033. Phone: (323) 865-0568. Fax: (323) 865-0570. E-mail: lieber{at}usc.edu.

{dagger} Supplemental material for this article may be found at http://mcb.asm.org/.

Molecular and Cellular Biology, January 2005, p. 294-302, Vol. 25, No. 1
0022-538X/05/$08.00+0     doi:10.1128/MCB.25.1.294-302.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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