Failure to produce mitochondrial DNA results in embryonic lethality in Rnaseh1 null mice
Open accessAbstract
Although ribonucleases H (RNases H) have long been implicated in DNA metabolism, they are not required for viability in prokaryotes or unicellular eukaryotes. We generated Rnaseh1(-/-) mice to investigate the role of RNase H1 in mammals and observed developmental arrest at E8.5 in null embryos. A fraction of the mainly nuclear RNase H1 was targeted to mitochondria, and its absence in embryos resulted in a significant decrease in mitochondrial DNA content, leading to apoptotic cell death. This report links RNase H1 to generation of mitochondrial DNA, providing direct support for the strand-coupled mechanism of mitochondrial DNA replication. These findings also have important implications for therapy of mitochondrial dysfunctions and drug development for the structurally related RNase H of HIV.
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In mice, an RNase H1 knockout is embryonic lethal at E8.5 when mtDNA replication begins.
“In mice, an RNase H1 knockout is embryonic lethal at E8.5 when mtDNA replication begins suggesting the mitochondrially located RNase H1 is essential for development (Cerritelli et al., 2003).”
From Role of the mitochondrial DNA replication machinery in mitochondrial DNA mutagenesis, aging and age-related diseases (2017) · cites this paper as Cerritelli et al., 2003
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References 47 · Cited by 358
- Authors
- Cerritelli, S. M., Frolova, E. G., Feng, C., Grinberg, A., Love, P. E., & Crouch, R. J.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Crouch, Robert J.
- Venue
- Molecular Cell
- Publisher
- Elsevier BV
- Published
- 2003-03
- Volume
- 11
- Issue
- 3
- Pages
- 807-815
- ISSN
- 1097-2765 (ISSN-L)
- OpenAlex
- W1967154926
- Cited by
- 358
- References
- 47
- Citations by year
- 2026: 14 · 2025: 15 · 2024: 23 · 2023: 13 · 2022: 20 · 2021: 21 · 2020: 22 · 2019: 26 · 2018: 12 · 2017: 15 · 2016: 17 · 2015: 15 · 2014: 20 · 2013: 13 · 2012: 14
- FWCI
- 4.71
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Molecular Cell (publishedVersion)
- PubMed (publishedVersion)
- Topics
- 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
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA Research and Splicing
- Keywords
- RNase H1, mitochondrial DNA replication, embryonic lethality, mitochondrial DNA content, apoptosis, mitochondrial dysfunction, HIV reverse transcriptase
- MeSH terms
- Alleles, Amino Acid Sequence, Animals, Cell Nucleus, DNA, DNA, Mitochondrial, Electron Transport, Genetic Vectors, Genotype, Homozygote, Mice, Inbred C57BL, Models, Genetic, Molecular Sequence Data, Plasmids, Time Factors, Blotting, Southern, Polymerase Chain Reaction, Ribonuclease H, Apoptosis, Mice, Knockout, In Situ Nick-End Labeling, Mice
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