Offices and Labs
Profile IntroductionGenetics of mammalian eye development
Genetic basis of mammalian eye development and congenital eye malformations
We study genetic mechanisms of vertebrate eye development, evolutionary conservation of gene networks, and transcriptional regulation. Our major interests include early patterning of the optic primordia and retinal cell fate specification. We use mutant and transgenic mice, human pedigrees segregating congenital eye malformations, and a variety of genomic, molecular and cell-based techniques. Current lab projects focus on ganglion cells – the first-born retinal neurons whose axons form the optic nerves and relay all visual information from the eye to the brain, fate symmetry, bHLH transcription factors, Notch signaling, the retinoid pathway, and molecular identification of new eye disease loci. Among these, we are investigating how mutations restricting retinoid (vitamin A) transport across the placenta cause maternally inherited eye malformations.
Department and Center Affiliations
CBS Grad Group Affiliations
Specialties / Focus
- Human Genetics and Genomics
- Animal Genomics
- Molecular Medicine
Heather Chapman, PhD
Farnaz Shoja-Taheri, PhD
Sean Woods, BS
Chou CM, Nelson C, Tarlé S, Pribila, J, Bardakjian T, Woods S, Schneider A and Glaser T. Biochemical basis for dominant inheritance, variable penetrance and maternal effects in RBP congenital eye disease, Cell 161, 634-646 (2015).
Prasov L and Glaser T. (2012) Dynamic expression of ganglion cell markers in retinal progenitors during the terminal cell cycle. Mol Cell Neurosci 50:160-168.
Prasov L and Glaser T. (2012) Pushing the envelope of retinal ganglion cell genesis: context dependent function of Math5 (Atoh7). Dev Biol 368:214-230.
Prasov L, Nagy M, Rudolph DD and Glaser T. Math5 (Atoh7) gene dosage limits retinal ganglion cell genesis. (2012) Neuroreport 23:631-634.
Prasov L, Masud T, Khaliq S, Mehdi SQ, Abid A, Oliver ER, Silva ED, Lewanda AF, Brodsky MC, Borchert M, Kelberman D, Sowden JC, Dattani MT and Glaser T. ATOH7 mutations cause autosomal recessive persistent hyperplasia of the primary vitreous. (2012) Hum Molec Genet 21:3681-3694.
Brzezinski JA, Prasov L and Glaser T. (2012) Math5 defines the ganglion competence state in a subpopulation of retinal progenitor cells exiting the cell cycle. Dev Biol 365:395-413.
Ghiasvand NM, Rudolph DR, Mashayekhi M, Brzezinski JA, Goldman DJ and Glaser T. (2011) Deletion of a remote enhancer for ATOH7 disrupts neurogenesis, causing nonsyndromic congenital retinal nonattachment. Nature Neurosci 14:578-586.
Prasov L, Brown NL and Glaser T. A critical analysis of Atoh7 (Math5) mRNA splicing in the developing mouse retina. (2010) PLoS ONE 5(8):e12315.
Saul SM, Brzezinski JA, Altshuler RM, Shore SE, Rudolph DD, Kabara LL, Halsey KE, Hufnagel RB, Dolan DF, Glaser T. (2008) Math5 expression and function in the central auditory system. Mol Cell Neurosci 37:153-169.
Brzezinski JA , Brown NL, Tanikawa A, Bush RA, Sieving PA, Vitaterna M, Takahashi J and Glaser T. (2005) Abnormal circadian behavior and retinal electrophysiology in Math5 mutant mice. Invest Ophthal Vis Sci 46:2540-2550.
Oliver ER, Saunders TL, Tarle SA and Glaser T. (2004) Ribosomal protein L24 defect in Belly spot and tail (Bst), a mouse Minute. Development 131:3907-3920.
Brown NL, Patel S, Brzezinski J, and Glaser T. (2001) Math5 is required for retinal ganglion cell and optic nerve formation. Development 128:2497-2508.
Tucker P, Laemle L, Munson A, Kanekar S, Oliver ER, Brown N, Schlecht H, Vetter M, and Glaser T. (2001) The eyeless mouse mutation (ey1) removes an alternative start codon from the Rx/rax homeobox gene. Genesis 31:43-53.