Mark Charlton-Perkins

 Mark Charlton-Perkins

Assistant Professor

390 Pearson Hall

Biographical Information

For more than 150 years, glial cells have been known to be a major part of neural tissue, but their role as the primary regulators of neural system development and function has only recently been understood. As glial cells' roles in neural homeostasis, metabolism, physiology, and structure become more appreciated, research into their development has increased. Genetic and microarray studies have identified several genes involved in glial cell proliferation, specification, activation, and regeneration. However, compared to their neuronal counterparts, which are much more numerous in the human brain, we still know very little about the final anatomical differentiation of glial cells. There are three active areas of investigation currently being pursued in my lab that focus either on the development or diseases in the nervous system.

We and others extensively studied the morphological and physiological changes of zebrafish retinal glia over their development, which has allowed us to categorize these cells into at least six progressive stages (Charlton-Perkins et al., McDonald et al., Wang et al.,). Using temporal transcriptomics combined with novel CRISPR strategies, we have developed methods to conduct large-scale reverse genetic screens and, for the first time, test the functions of these differentiation factors in mass. These developmental studies aim to identify evolutionarily conserved pathways responsible for both glial cell shape and the development of their mature physiologies. This research has far-reaching implications for our understanding of cellular evolution. It provides novel insights into the process of evolution and can influence studies on many genes related to neural diseases. In particular, we have developed three disease models (Wolfram’s Disease, Neuromyelitis Optica and Neurofibromatosis type-1) that further explore how these highly conserved molecular pathways are implicated in gliopathies.  This research could help to identify the genetic basis of certain neurological diseases, as well as provide new ways of treating them.

Courses Taught

  • BIO 203: Cell Biology
  • BIO 710: Seminar in Biology: Neural Glial Development

Selected Publications

  • Charlton-Perkins MA, Cook TA, Friedrich M. Semper's Cells in the Insect Compound Eye: Insights into Ocular Form and Function (2021). Developmental Biology S0012-1606 (21)00178-0. doi: 10.1016/j.ydbio.2021.07.015

  • Charlton-Perkins M, Almeida AD, MacDonald RB, Harris WA. Genetic control of cellular morphogenesis in Müller glia (2019). GLIA 67(7): 1401-1411

  • MacDonald RB, Charlton-Perkins M, Harris WA. Mechanisms of Müller glial cell morphogenesis (2017). Current Opinions in Neurobiology 47:31-37

  • Charlton-Perkins MA, Sendler ED, Buschbeck EK, Cook TA. Multifunctional glial support by Semper cells in the Drosophila retina (2017). PLoS Genetics 31;13(5)

  • Eldred MK, Charlton-Perkins M, Muresan L, Harris WA. Self-organising aggregates of zebrafish retinal cells for investigating mechanisms of neural lamination (2017). Development 144(6):1097-1106

  • Stahl AL, Charlton-Perkins M, Buschbeck EK, Cook TA. The cuticular nature of corneal lenses in Drosophila melanogaster (2017). Development Genes and Evolution 227(4):271-278.

  • Luebbering N, Charlton-Perkins M, Kumar JP, Rollmann SM, Cook T, Cleghon V (2013). Drosophila Dyrk2 plays a role in the development of the visual system. PLoS One 11,8(10).

  • Jukam D, Xie B, Rister J, Terrell D, Charlton-Perkins M, Pistillo D, Gebelein B, Desplan C, Cook T (2013). Opposite feedbacks in the Hippo pathway for growth control and neural fate. Science Oct 11;342.

  • Charlton-Perkins, M., Brown, N.L., and Cook, T.A (2011). The lens in focus: a comparison of lens development in Drosophila and vertebrates. Molecular Genetics and Genomics 286, 189-213.

  • Charlton-Perkins, M., Whitaker, S.L., Fei, Y., Xie, B., Li-Kroeger, D., Gebelein, B., and Cook, T (2011). Prospero and Pax2 combinatorially control neural cell fate decisions by modulating Ras- and Notch-dependent signaling. Neural Development 6, 20.