EndoG is dispensable in embryogenesis and apoptosis
Abstract
The mitochondrial protein, endonuclease G (EndoG), is one of the endonucleases implicated in DNA fragmentation during apoptosis. It has been shown to translocate from the mitochondria to the nucleus upon cell death stimuli. These observations suggest that EndoG is a mitochondrial cell death effector, and that it possibly acts as a cell death nuclease, similar to DNA fragmentation factor. To better understand the role of EndoG in development and apoptosis, we generated EndoG null mice by homologous gene targeting without disruption of D2Wsu81e. EndoG null mice are viable and develop to adulthood with no obvious abnormalities. Fibroblasts generated from the EndoG null mice show no difference in susceptibility when induced to die by a variety of intrinsic and extrinsic apoptotic stimuli. Additionally, EndoG null mice are equally sensitive to excitotoxic stress. These data suggest that EndoG is not essential for early embryogenesis and apoptosis.
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The actual contribution of ENDOG to RCD in mammals has been questioned by generation of Endog−/− mice, whose cells display normal sensitivity to multiple lethal triggers.
“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 [676]
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- Authors
- David, K. K., Sasaki, M., Yu, S.-W., Dawson, T. M., & Dawson, V. L.
- Affiliations
- Johns Hopkins University (US)
- Corresponding author
- Dawson, V L
- Venue
- Cell Death & Differentiation
- Published
- 2005-10-21
- Volume
- 13
- Issue
- 7
- Pages
- 1147-1155
- ISSN
- 1350-9047 (ISSN-L)
- 1476-5403
- OpenAlex
- W2018825568
- Cited by
- 96
- References
- 38
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 4 · 2023: 5 · 2022: 4 · 2020: 6 · 2019: 2 · 2018: 3 · 2017: 1 · 2016: 2 · 2015: 4 · 2014: 4 · 2013: 4 · 2012: 8
- FWCI
- 1.99
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Cell Death and Differentiation (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Public Health Service
- National Institute of Neurological Disorders and Stroke (NS039148, P01NS039148)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Keywords
- endonuclease G, embryonic development, apoptosis, DNA fragmentation, mitochondrial cell death, fibroblasts, gene targeting
- MeSH terms
- Animals, Brain, Cell Nucleus, Cells, Cultured, Dose-Response Relationship, Drug, Endodeoxyribonucleases, Etoposide, Female, Fibroblasts, Immunohistochemistry, Methylnitronitrosoguanidine, Mice, Inbred C57BL, Mice, Inbred Strains, Mitochondria, Pregnancy, Tumor Necrosis Factor-alpha, Apoptosis, Mice, Knockout, Reverse Transcriptase Polymerase Chain Reaction, Embryonic Development, Apoptosis Inducing Factor, Mice
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