Levinger L, O Jacobs*, M James*. 2001. In vitro 3' end endonucleolytic processing defect in a human mitochondrial tRNASer(UCN) precursor with the U7445C substitution, which causes non-syndromic deafness. Nucleic Acids Res. 29:4334-4340. — by Louis Levinger — last modified Feb 21, 2008 09:04PM

In this paper (published in Nucleic Acids Research), we demonstrated that the defect in a mutant mitochondrially encoded pre-tRNA associated with non-syndromic deafness is in the 3' end processing by tRNase Z. Student co-authors (Obasanjo Jacobs and Melissa James) continued in their professional education (DO School and PhD in Cell and Molecular Biology) after receiving research laboratory training with Dr. Levinger

Levinger, L., Giegé, R., Florentz, C. 2003. Pathology-related substitutions in human mitochondrial tRNAIle reduce precursor 3' end processing efficiency in vitro. Nucleic Acids Res. 31:1904-1912. — by Louis Levinger — last modified Feb 21, 2008 09:04PM

This publication in Nucleic Acids Research is the first of a series based on Dr. Levinger's sabbatical with Catherine Florentz and Richard Giege at the Institute for Cellular and Molecular Biology in Strasbourg, France from 2001-2002. The general topic of the sabbatical research was precursor tRNA 3' end processing and mitochondrially transmitted human diseases. The research was supported by a fellowship from the NIH.

Unpublished Work

Transfer RNA (tRNA) is a small nucleic acid molecule involved in protein synthesis. tRNAs are transcribed as precursors and tRNase Z is the enzyme that cleaves off the pre-tRNA 3' end trailer. tRNase Z has a flexible domain (FD, pictured) that is remote from the active site of the enzyme and is involved in substrate recognition and binding. The FD is under investigation in the Levinger lab, and is the topic of two pending grant proposals.