Stacey Glasgow

Research

Glia are the most abundant cell type in the adult central nervous system (CNS) and support a diverse array of physiological functions including myelination, synaptogenesis, neurotransmission, and blood-brain barrier maintenance. Consistent with this functional heterogeneity, disruptions in normal gliogenesis and glial maintenance have been reported as defining events in the onset and progression of several neurological disorders and malignancies. Despite their essential and emerging roles in CNS functions and pathologies, the molecular mechanisms that govern glial cell specification from neural progenitors and how these mechanisms are correlated with associated diseases are poorly defined. Specification and lineage commitment involves coordinated gene expression regulated by chromatin remodeling, transcriptional cascades, and binding site recognition. Understanding how these regulatory layers converge to influence gene expression remains a key question with implications in neural development, function, and associated disease.

In my laboratory, we use interdisciplinary approaches to study both glial development and ultimately, neurodegenerative diseases and glioma. Specifically, we are interested in dissecting the mechanisms underlying transcriptional regulation and chromatin architecture of glial cell development and applying these developmental concepts to glioma tumorigenesis. Methodologically, we utilize manipulation of both chick and mouse model systems in combination with biochemical and transcriptional assays to help elucidate these molecular underpinnings.

Select Publications

  • Laug D, Glasgow SM, Deneen B. (2018) A glial blueprint for gliomagenesis. Nature Reviews Neuroscience. Jul;19(7):393-403.
  • Glasgow SM, Carlson J, Zhu W, Kang P, Chaboub LS, Lee HK, Clovis Y, Lozzi B, McEvilly RJ, Rosenfeld MG, Creighton C, Lee SK, Mohila C, Deneen B. (2017) Glial specific enhancers and chromatin structure regulate NFIA expression and glioma tumorigenesis. Nature Neuroscience 11: 1520-1528.
  • Chaboub LS, Manalo JM, Lee HK, Glasgow SM, Chen F, Kawazaki Y, Akiyama T, Creighton CJ, Mohila CA and Deneen B. (2016) Temporal profiling of astrocyte precursors reveals parallel roles for asef during development and after injury. Journal of Neuroscience 36(47): 11904-11917.
  • Thiebes K, Nam H, Cambronne X, Shen R, Glasgow SM, Cho H, Kwon J, Goodman R, Lee JW, Lee SH, Lee SK (2015) miR-218 is essential to establish motor neuron fate as a downstream effector of Isl1-Lhx3. Nature Communications 6.
  • Glasgow SM, Zhu W, Stolt CC, Huang TW, Chen F, LoTurco JJ, Neul JL, Wegner M, Mohila C, Deneen B. (2014) Mutual antagonism between Sox10 and NFIA regulates diversification of glial lineages and glioma subtypes. Nature Neuroscience 17: 1322-1329.
  • Glasgow SM, Laug D, Brawley V, Zhang Z, Corder A, Yin Z , Wong STC, Li XN, Foster AE, Ahmed A, and Deneen B. (2013) The miR223-NFIA Axis Regulates Glial Precursor Proliferation and Tumorigenesis in the CNS. Journal of Neuroscience 33(33): 13560-13568. **Featured in Science “Editor’s Choice” http://www.sciencemag.org/content/341/6150/1044.4.short
  • Molofsky A*, Glasgow SM*, Chaboub L, Tsai H-H, Murnen AT, Fancy SF, Yuen T, Mahireddy L, Baranzini S, Deneen B, Rowitch DH, Oldham M. (2013) Expression profiling of putative astrocyte precursors in the developing spinal cord identifies Sox9-Nfe2l1 interactions. Glia 61(9):1518-32.
  • Fancy SF*, Glasgow SM*, Finley M, Rowitch DH, and Deneen B (2012) Evidence that NFIA inhibits repair after white matter injury. Annals of Neurology 72(2):224-233.
  • Kang P*, Lee HK*, Glasgow SM, Finley M, Donti T, Gaber ZB, Graham BH, Foster AE, Novitch BG, Gronostajski RM, and Deneen B (2012) Sox9 and NFIA coordinate a transcriptional regulatory cascade during the initiation of gliogenesis. Neuron 74(1):79-94.
  • Henke RM, Savage TK, Meredith DM, Glasgow S.M., Hori K, Dumas J, MacDonald RJ, and Johnson JE. (2009) Neurog2 is a Direct Downstream Target of the Ptf1a-Rbpj Transcription Complex in Dorsal Neural Tube. Development 136, 2945-2954
  • Hori K, Cholewa-Waclaw J, Nakada Y, Glasgow SM, Masui T, Henke RM, Wildner H, Martarelli B, Beres TM, Epstein JA, Magnuson MA, Macdonald RJ, Birchmeier C, Johnson JE. A nonclassical bHLH Rbpj transcription factor complex is required for specification of GABAergic neurons independent of Notch signaling. Genes Dev. 2008 Jan 15; 22(2):166-78.
  • Glasgow, SM, Henke, RM, MacDonald, RJ, Wright, C, Johnson, JE (2005) PTF1a Specifies Dorsal Horn GABAergic Over Glutamatergic Cell Fate. Development 132, 5461-5469