Qiang Chang
Assistant Professor
- Address:
- 659 Waisman Center
- Telephone:
- 262-9416
- Email:
- qchang@waisman.wisc.edu
- Research Fields:
- Mouse Genetics
- Neurogenetics
- Developmental Genetics
Ph.D. University of Pennsylvania School of Medicine, 2000
Postdoctoral Research: Whitehead Institute, Cambridge, MA
Research Interests
Epigenetic regulation of brain functions
Research Description
Research in my laboratory is aimed at understanding the molecular mechanism of Rett syndrome, an autistic spectrum developmental disorder, and DNA methylation dependent epigenetic regulation of mammalian brain development and function.
Rett syndrome is caused by mutations in the X-linked MECP2 (methyl CpG binding protein 2). The devastating disease has an estimated prevalence of 1 in 10,000-15,000 girls, and is the second most common cause of mental retardation in females. MeCP2 plays a central role in interpreting the epigenetic code of DNA methylation and regulating chromatin remodeling and gene transcription in the mouse brain.
We employ mouse genetics, electrophysiological, and molecular approaches to:
- Identify MeCP2 target genes.
- Elucidate the mechanisms by which MeCP2 dynamically regulate the expression of these genes.
- Characterize the in vivo roles of these genes in the context of RTT and normal brain development.
Representative Publications
- Chang, Q., Khare, G.D., Dani, V.S., Nelson, S.B., and Jaenisch, R. (2006) The disease progression of Mecp2 mutant mice is affected by the level of BDNF expression. Neuron 49(3):341-348.
- Dani, V.S.*, Chang, Q.*, Maffei, A., Turrigiano, G.G., Jaenisch, R., and Nelson, S.B. (2005) Reduced cortical activity due to a shift in the balance between excitation and inhibition in a mouse model of Rett Syndrome. PNAS 102(35):12560-12565. (* Equal contribution)
- Chen, W.G., Chang, Q., Lin, Y., Meissner, A., West, A.E., Griffith, E.C., Jaenisch, R., and Greenberg, M.E. (2003) Derepression of BDNF transcription involves calcium-dependent phosphorylation of MeCP2. Science 302:885-889.