| First Author | Cerritelli SM | Year | 2003 |
| Journal | Mol Cell | Volume | 11 |
| Issue | 3 | Pages | 807-15 |
| PubMed ID | 12667461 | Mgi Jnum | J:82764 |
| Mgi Id | MGI:2655010 | Doi | 10.1016/s1097-2765(03)00088-1 |
| Citation | Cerritelli SM, et al. (2003) Failure to produce mitochondrial DNA results in embryonic lethality in Rnaseh1 null mice. Mol Cell 11(3):807-15 |
| abstractText | 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. |
