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Generation and Characterization of Endonuclease G Null Mice
Open accessAbstract
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.
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“the actual contribution of ENDOG to RCD in mammals [675] has been questioned by the generation of Endog−/− mice, whose cells display normal sensitivity to multiple lethal triggers [676, 677].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [677]
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Metadata
- Authors
- Irvine, R. A., Adachi, N., Shibata, D. K., Cassell, G. D., Yu, K., Karanjawala, Z. E., Hsieh, C.-L., & Lieber, M. R.
- Affiliations
- University of Southern California (US)
- Departments of Pathology, of Biochemistry & Molecular Biology, of Molecular Microbiology & Immunology, and of Biological Sciences
- Corresponding author
- Lieber, Michael R.
- Venue
- Molecular and Cellular Biology
- Publisher
- Informa UK Limited
- Published
- 2005-01
- Volume
- 25
- Issue
- 1
- Pages
- 294-302
- ISSN
- 0270-7306 (ISSN-L)
- 1098-5549
- PMC
- PMC538798
- OpenAlex
- W2125483893
- Cited by
- 111
- References
- 30
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 3 · 2023: 4 · 2022: 1 · 2021: 4 · 2020: 2 · 2019: 1 · 2018: 2 · 2017: 1 · 2016: 5 · 2015: 3 · 2014: 2 · 2013: 7 · 2012: 6
- FWCI
- 3.67
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Molecular and Cellular Biology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute of General Medical Sciences (R01GM056984)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Keywords
- endonuclease G, gene knockout, mitochondrial DNA, mitochondrial intermembrane space, nuclease activity, mitochondrial DNA copy number, apoptosis, nuclear DNA degradation, embryonic lethality
- MeSH terms
- Animals, Cell Nucleus, Cell Survival, Chromatin, DNA, DNA, Mitochondrial, Endodeoxyribonucleases, Enzyme-Linked Immunosorbent Assay, Immunoglobulin G, Immunoglobulin M, Mice, Inbred C57BL, Mice, Mutant Strains, Mice, Transgenic, Mitochondria, Models, Genetic, Mutation, Plasmids, Spleen, Blotting, Southern, Blotting, Western, Apoptosis, Transgenes, Mice, DNA Fragmentation
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