Failure to produce mitochondrial DNA results in embryonic lethality in Rnaseh1 null mice

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Abstract

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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Cerritelli, S. M., Frolova, E. G., Feng, C., Grinberg, A., Love, P. E., & Crouch, R. J. (2003). Failure to produce mitochondrial DNA results in embryonic lethality in Rnaseh1 null mice. Molecular Cell, 11(3), 807–815. https://doi.org/10.1016/S1097-2765(03)00088-1

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