Post Doctoral Fellowships
Juan I. Young, Ph.D.
Baylor College of Medicine
Mentor: Huda Zoghbi, M.D.
"Is Rett Syndrome Reversible? Conditional Restoration of MeCP2 Function in a Mouse Model for Rett Syndrome"
2-Year Award: $100,000
Recipient of the Alan P. Wolffe Memorial Fellowship
Lay Progress Report (August, 2004)
MeCP2 mutant mice display a neurological phenotype. To test for the reversibility of this phenotype, we have generated transgenic mice in which MeCP2 could be turned ON and OFF specifically on certain regions of the brain on demand. Mice mutant for the endogenous Mecp2 gene, that carry the exogenous MeCP2 transgene in its ON version, displayed some improvement, indicating that the transgene is functional. However, the lack of a complete prevention of the phenotype suggests that modifications of transgene expression patterns are necessary. We are generating new mice that will express the transgenic MeCP2 in every neuron in which the endogenous gene is supposed to be present in order to test for a full rescue of the phenotype.
Juan I. Young, Ph.D.Baylor College of Medicine
Mentor: Huda Zoghbi, M.D.
"Is Rett Syndrome Reversible? Conditional Restoration of MeCP2 Function in a Mouse Model for Rett Syndrome"
2-Year Award: $100,000
Recipient of the Alan P. Wolffe Memorial Fellowship
Lay Progress Report (August, 2004)
MeCP2 mutant mice display a neurological phenotype. To test for the reversibility of this phenotype, we have generated transgenic mice in which MeCP2 could be turned ON and OFF specifically on certain regions of the brain on demand. Mice mutant for the endogenous Mecp2 gene, that carry the exogenous MeCP2 transgene in its ON version, displayed some improvement, indicating that the transgene is functional. However, the lack of a complete prevention of the phenotype suggests that modifications of transgene expression patterns are necessary. We are generating new mice that will express the transgenic MeCP2 in every neuron in which the endogenous gene is supposed to be present in order to test for a full rescue of the phenotype.