Biography
- Research Assistant Professor, Pediatrics (Surgery), Department of Ophthalmology, Ann & Robert H. Lurie Children's Hospital of Chicago
Dr. Williams' research focuses on neural crest contributions to the vertebrate eye utilizing zebrafish ocular disease models to identify essential factors involved in the regulation of eye development from the anterior segment to the choroid. These studies will improve our understanding of the pathophysiology of blinding diseases as a foundation for the development of molecularly targeted treatments and therapies for the prevention of blindness and restoration of vision in patients with ophthalmic abnormalities.
Education and Background
- Postdoctoral fellowship, molecular and integrative physiology 2008–2010
- PhD, cell and molecular biology, University of Michigan Medical School 2008
- BS, microbiology, University of Michigan 1997
- AS, biochemistry, St. Clair County Community College 1994
Research Highlights
THE ROLE OF NEURAL CREST CELLS IN OCULAR DEVELOPMENT FROM THE ANTERIOR SEGMENT TO THE CHOROID
Eye development greatly depends on neural crest cells to form many of its structures. In this project, we use zebrafish models to expand the current knowledge of periocular neural crest contributions to eye development from the anterior segment and beyond to improve our mechanistic understanding of ocular morphogenesis and the pathogenesis of ophthalmic diseases. The prevalence of visual impairments and blinding diseases in human society is a critical concern on a global scale, with almost half of these cases representing potentially preventable instances or defects that have yet to be addressed. Assessment of the shared pathophysiological defects among these ocular disorders highlights the persistent need for a thorough and comprehensive understanding of ocular morphogenesis. Indeed, defining the mechanisms underlying normal eye development is paramount to inform the pathophysiology of ocular diseases and improve diagnostic and therapeutic strategies.
We and others have extensively shown that eye development is exquisitely sensitive to the proper development of the neural crest. As an embryonic stem cell population, the neural crest detects a variety of signals for their migration, proliferation, and differentiation into diverse cells and tissues. In addition, neural crest cells can also influence the development of surrounding tissues in the eye, even though they themselves do not directly become part of those tissues. However, the specific interactions between the dynamic periocular neural crest and its surrounding environment during normal eye development remain undefined. Using a combination of molecular, cellular, and developmental biology techniques with genetic manipulation, advanced microscopy and live imaging techniques in zebrafish models, we will elucidate the precise mechanisms by which the periocular neural crest influences cell behaviors during ocular morphogenesis.
THE MECHANICS OF NEURAL CREST BIOLOGY IN CORNEAL DEVELOPMENT AND OCULAR WOUND HEALING
A critical barrier in developing vision-saving strategies for ophthalmic injury repair is the limited knowledge of the cellular changes underlying the destruction of normal cellular architecture and replacement with scar tissue leading to fibrosis. Notably, many features of ophthalmic regeneration recapitulate those of ocular development. The goal of this research is to better understand the biology of embryonic neural crest cells as it pertains to understanding anterior segment development, with particular emphasis on corneal development, and determining whether the same pathways play a role in the regeneration of their adult derivatives upon corneal injury.
I initiated these studies by employing RNA sequencing technology and embryonic and adult zebrafish models to identify and characterize additional factors involved in embryonic ocular neural crest development and examine potential roles for these factors in postnatal ocular injury repair. Ultimately, new knowledge about the signals that direct these neural crest-derived corneal tissues to regenerate instead of scar or degenerate will lead to molecularly targeted therapies that prevent vision loss.
