The NIH has placed a priority on discovering the function of genes identified through the human genome project. The mouse has been recognized as the pre-eminent organism to model human disease and various initiatives have focused on its use in this regard. One powerful means to illuminate gene function is through mutagenesis, and the NIMH and other neurological institutes have funded three centers to carry out chemical mutagenesis in the mouse and screen mice for neuroscience-related phenotypes. To make these centers of core use to the neuroscience community, each center must attract researchers to use the mutagenesis facilities for their research programs. The Tennessee Mouse Genome Consortium (TMGC), a group of eight institutions across the State of Tennessee, is one of the three funded centers and proposes a plan to recruit researchers and students to maximize the potential of our neuromutagenesis program and train individuals in the use of mutant mice for neuroscientific endeavors. We have three components of our training and education plan. First, we will actively work to recruit investigators who demonstrate an abiding interest in applying new phenotyping protocols to our mutant mice. This may represent a new direction for some or a realization of the power of genetic analysis for others, but in all cases we will work with them to understand the basics of our program and to obtain sustained funding for these efforts. Second, we will establish a training program for undergraduate and graduate students and postdoctoral fellows in the behavioral analysis of mutant mice using the TMGC neuromutagenesis program. Finally, we propose to offer an annual workshop-style course in neurogenetics and analysis of mouse behavior. Through these three mechanisms, we plan to create a new pool of researchers that understand the power of neurogenetic approaches and can take advantage of neurological mutant mice in understanding brain structure and function.
| Matthews, Douglas B; Chesler, Elissa J; Cook, Melloni N et al. (2008) Genetic mapping of vocalization to a series of increasing acute footshocks using B6.A consomic and B6.D2 congenic mouse strains. Behav Genet 38:417-23 |
| Thornton, J Derek; Swanson, Doug J; Mary, Michelle N et al. (2007) Persistent hyperplastic primary vitreous due to somatic mosaic deletion of the arf tumor suppressor. Invest Ophthalmol Vis Sci 48:491-9 |
| Hamre, Kristin M; Goldowitz, Daniel; Wilkinson, Sarah et al. (2007) Screening for ENU-induced mutations in mice that result in aberrant ethanol-related phenotypes. Behav Neurosci 121:665-78 |
