 Joseph Nadeau, PhD
jhn4@cwru.edu
Phone: 216 368-0581
Biography
Joseph Nadeau received his Ph.D. in population biology from Boston University in 1978. He was a postdoctoral fellow with Jan Klein in the Immunogenetics Department, Max Planck Institute for Biology, Tübingen (1978-1980) and with Eva Eicher at the Jackson Laboratory (1980-1981). He was appointed Associate Staff Scientist (1981-1985), Staff Scientist (1985-1991) and Senior Staff Scientist (1991-1994) at the Jackson Laboratory, and then Professor, Department of Human Genetics, McGill University and Medical Scientist, Department of Medicine, Montreal General Hospital (1994-1996). He is currently Professor, Genetics Department Case Western Reserve University School of Medicine. He was a founding member of the International Mammalian Genome Society and a founding editor of Mammalian Genome. He was founder and director of the Mouse Genome Informatics Project (1989-1994) and founder of the Mouse Gene Expression Database Project (1992-1994). He has served on review panels and advisory groups at the National Institutes of Health, the National Science Foundation and the Human Genome Database. He is currently a member of the SmithKline Beecham Bioinformatics Advisory Board and the National Advisory Council for Human Genome Research.
Research Interests
Many common human diseases are complex involving various combinations of genes and environmental factors. While remarkable research progress is being made in humans, models from laboratory mice are important because they provide an experimental system for identifying disease genes, the physiological and developmental pathways in which these genes function, and interactions among these genes and environmental factors We use a combination of genetic, developmental, molecular, genomic and mathematical methods for studying these problems.
Our research focuses on the genetic and phenotypic dissection of selected mouse models of human multifactorial disease traits. The goal of this work is to develop general methods for analyzing complex traits in experimental systems and learn about the particular disease models. These studies use a combination of expression assays for large numbers of genes, measurement of metabolite levels and enzyme activities in normal and variant mice with emphasis on folate metabolism and inositol phospholipid metabolism, and linkage analysis of genes controlling these traits as well as disease susceptibility genes. With these various assays, we have identified new mouse models for hyperhomocysteinemia or reduced methylenetetrahydrofolate reductase (MTHFR) activity in mice with neural tube defects, exencephaly, cardiovascular disease, or generalized seizures. In addition we have identified anomalies in gene expression profiles in these mice and we have begun to define new networks of gene expression control. Other current work focuses on positional cloning and characterization of the Disorganization mutation, a single gene that causes an extra-ordinary variety of birth defects, the genetic control of susceptibility to testicular germ cell tumors, and the genetic and developmental control of drug-induced birth defects. His laboratory is developing new kinds of mouse genetic resources for complex trait analysis. Finally, he has pioneered the mathematical analysis of comparative genetic maps as a means for studying genome organization and evolution. Current work focuses on the evolution of gene families and physiological pathways. Click here to view/download lab data.
Publications
- Nadeau, J. H. and B. A. Taylor, 1984. Lengths of chromosomal segments conserved since divergence of man and mouse. Proc. Natl. Acad. Sci. USA 81:814-818.
- Nadeau, J. H. 1991 Genome Duplication and Comparative Gene Mapping. In Advanced Techniques in Chromosome Research. K. Adolph, ed. pp 269 296. Marcel Dekker, New York.
- Crosby, J.L., D.S. Varnum, and J.H. Nadeau 1993. Two-hit model for sporadic congenital anomalies in mice with the disorganization mutation. Am. J. Hum. Genet. 52:866-874.
- Asada, Y., D.S. Varnum, W.N. Frankel, and J.H. Nadeau 1994. A mutation in the Ter gene causing increased susceptibility to testicular teratomas maps to mouse chromosome 18. Nature Genetics 6:363-368.
- Helwig, U., K. Imai, M. Schmahl, B.E. Thomas, D.S. Varnum, J.H. Nadeau, and R. Balling 1995. Interaction between undulated and Patch leads to an extreme form of spina bifida in double mutant mice. Nature Genetics 11:60-63.
- Rozmahel, R., M. Wilschanski, A. Matin, S. Plyte, M. Oliver, W. Auerbach, A. Moore, J. Fostner, P. Durie, J.H. Nadeau, C. Bear, and L.-C. Tsui 1996 Modulation of disease severity in CF mice by a secondary genetic factor. Nature Genet 12:280-287.
- Sankoff, D., and J.H. Nadeau 1996 Conserved synteny as a measure of genomic distance. Discrete Appl. Math. 71: 247-257.
- Ernest, S.R., B. Christiansen, B.M. Gilfix, O.A. Mamer, P.J. Dunn, A. Hosack,
M. Rodier, C. Colmenares, J. McGrath, A. Bale, R. Balling, D. Rosenblatt and
J.H. Nadeau 200_ Genetic, molecular and physiological control of folate
and homocysteine metabolism in mutant mice. Mammal. Genome (in press).
- Hoit, B.D., S. Kiatshoosakun, J. Restivo, D. Kirkpatrick, H. Shao, K.
Olszens, Y.-H. Pao and J.H. Nadeau 200_ Naturally occurring variation in
cardiovascular traits among inbred mouse strains: a mouse model of the athlete’s
heart. Genomics (in press).
Links
Genetics
|
