• Ph.D.- Columbia University, Biological Sciences/Molecular Biology
• M.Ph.- Columbia University, Biological Sciences/Molecular Biology
• M. A.- Columbia University, Biological Sciences/Molecular Biology
• A.B. - University of Chicago, Biology

Semester System
• BIOL 1505: Biology and the Modern World
• BIOL 2601: Principles of Biology 1
• BIOL 2621: Genetics
• BIOL 6963: Virology

My laboratory works on two projects involving mitochondrial DNA. In addition, I am involved in several projects in feline genetics.

Mitochondria are small organelles that function as the biological powerhouses of the cell. Mitochondria contain their own genome (mtDNA) which replicates independently of the cycles that control chromosomal DNA replication in the nucleus. Defects in mitochondrial DNA (mtDNA) are being increasingly implicated in a variety of degenerative human diseases.

Little is currently known about the relative transmission of normal and mutant mtDNAs, or about the control of mtDNA replication in general. The yeast Saccharomyces cerevisiae presents a system where competitive transmission of wild-type and mutant mtDNAs is quite accessible to analysis. Some mutant yeast mtDNAs are preferentially inherited. There are human diseases caused by mtDNA mutations. Some of these mtDNAs also appear to have a replication advantage that contributes to disease processes. We use a 2-dimensional gel electrophoretic procedure to analyze DNA structure to help elucidate the mechanism by which certain types of mtDNA mutations effect inheritance. Additionally, in collaboration with Dr. Ian Holt at Ninewells Hospital in Dundee Scotland, we are examining the general structure and replicating of both normal and disease causing mutants of human mitochondrial DNA. Ultimately this work may lead to more basic understanding of the process of mtDNA replication and how it is regulated.

The state of genetic information on small felids is still scarce compared to that available on humans and the major laboratory organisms. More complete information will be of enormous use to veterinarians, cat fanciers, and biologists working with endangered wild cats. I am involved with collecting and analyzing data on feline genetic diversity and inheritance of a number of feline diseases and visible feline traits. Most of this work is facilitated by using the extensive information available on pedigreed cats from those within the Cat Fanciers Association.
 

Publications

Holt, I.J., H. E. Lorimer, and H.T. Jacobs. 2000. Coupling leading- and lagging- strand synthesis of mammalian mitochondrial DNA. Cell 100: 515-524.

Lorimer, H. E., B. Brewer, and W. L. Fangman. 1995. A test of the transcription model for the biased inheritance of yeast mitochondrial DNA. Mol. Cell. Biol. 15 (9):4803-4809.

Lockshon, D., S. G. Zweifel, L. L. Freeman, H. E. Lorimer, B. J. Brewer, and W. L. Fangman. 1995. A role for recombination junctions in the segregation of mitochondrial DNA in yeast. Cell 81:947-955.

Reynisdottir*, I., H. E. Lorimer*, P. N. Friedman, E. H. Wang, and C. Prives. Phosphorylation and active ATP hydrolysis are not required for SV40 T antigen hexamer formation. 1993. J. Biol. Chem. 268(33):24647-24654. (*The first two authors contributed equally to this report)

Lorimer, H. E., I. Reynisdottir, S. Ness, and C. Prives. 1993. Unusual Properties of a replication-defective mutant SV40 large T antigen. Virology 192:402-414.