Lab Members

I have been an associate research scientist in John Lab since February of 2019. I earned my Ph.D. in Developmental Biology from Fudan University in 2012 where I used different mouse models to investigate heart, kidney and retinal diseases. Since joining the John lab, my focus has been on developing inducible glaucoma mouse models as well as molecular mechanism of neural damage in glaucoma.

I joined the John lab in September of 2018 as a research assistant. I earned my BS in Physiology & Neurobiology from the University of Connecticut in 2017. I have experience with behavioral assays, ocular phenotyping of mice, immunohistochemistry, data visualization with R, and computer-aided design.

I received my Bachelor of Science in Neuroscience with a concentration in Molecular and Cellular Biology from the Johns Hopkins University in 2017. My main research interests are genetics and neuroscience. As an undergraduate, I worked in Seth Blackshaw's lab on a project entitled "Investigating the role of Lhx2 in the development of the ciliary body." Since graduating college, I have worked in several labs ranging from studying blood diseases to building a library of nuclear constructs to study the phase separation of nuclear proteins in vivo. I am experienced in tissue culture, mouse husbandry, cloning, and various molecular biology techniques. I joined the John lab in June of 2020 as a Research Associate. During my free time I enjoy reading, exploring new areas in New York, and spending time with my dog, Nova.

I received my B.A. in Behavioral Neuroscience from Connecticut College . During my time at Connecticut College, I worked on several different research projects. We studied whether Ceftriaxone and other β-lactam antibiotic compounds could attenuate morphine reward in rats by enhancing the reuptake rate of excitatory amino-acid transporters. For my honors thesis, I examined the effects of developmental lead exposure on working memory performance in rats after manipulating several elements of the animal’s developmental environment.

I started my Ph.D. in the John lab in 2016. I am studying the roles of a LIM domain transcription factor , LMX1b, in ocular development and adult-onset glaucoma. This has allowed me an unusually broad graduate training including clinical, molecular, genetic, genomic, and other computational/statistical approaches using R, Seurat and other software. Beyond immunohistochemistry and other standard molecular techniques, I have mastered various delicate dissections (retina, optic nerve, brain regions and ocular drainage tissues) and precise ocular physiological measurements (including intraocular pressure and ocular fluid drainage or outflow). My projects have also involved clinical and histologic examination of mouse eyes and Mendelian and complex genetics including the diversity outbred mouse population. I have been involved with several other exciting projects, including the screening for and characterization of high IOP mutants and in a collaboration with engineers towards developing new treatment tools. Currently, I am focusing on the developmental biology of ocular development in Lmx1b mutants as well as the gene expression networks controlling ocular development and IOP elevation (using single cell sequencing, bulk RNA sequencing and other approaches). Dr. John has facilitated my interaction with collaborators and exposed me to grant writing, lab. management decisions and strategic planning. This diverse training along with his mentorship and the lab's environment are putting me in a strong position for my future career as a PI.

Being from coastal Maine, I was used to being an outdoor person at our lab's initial location next to Acadia National Park. The exciting and fast paced environment at our new location, Columbia University, is an amazing experience with the opportunity to learn from many first-rate scientists.

Dr. Morgan's research is aimed at understanding the structural and cellular changes occurring at the level of the optic nerve in glaucoma using clinical and laboratory-based techniques. Glaucoma is one of the most common causes of vision loss in the UK population, affecting up to 2% of the population. Classically, it is associated with increased intraocular pressure, which causes the death of retinal ganglion cells and results in a slow and, if untreated, progressive loss of vision. In most cases, peripheral vision is lost first and is usually asymptomatic. By the time a patient notices restriction of visual field, advanced damage may have occurred to the optic nerve that is usually irreversible. Treatment is aimed at the reduction of eye pressure (intraocular pressure) to prevent this vision loss. Usually, this is achieved using eye drops although, in some cases, surgery or even laser treatment may be required. One of the key problems is in identifying the disease in its earliest stages and in detecting the first signs of retinal (optic nerve) damage. As a consultant ophthalmologist, Morgan runs a glaucoma service at the University Hospital of Wales. He currently chairs the Expert Working Group for the development of shared care glaucoma in Wales where they are working to develop the role of virtual clinics for the community care of patients with diagnosed glaucoma. His email address is MorganJE3@cardiff.ac.uk.

Clinical Studies: 

These are based at the Retinal Imaging Laboratory and are directed at the quantification of structural optic nerve changes in the early stages of glaucoma. Since these precede the development of visual field changes as detected using clinical perimetric techniques, their detection should enable early disease diagnosis and improve the long-term prognosis for the patient. Morgan's lab is currently assessing the value of digital stereoviewing in the quantification of these nerve head changes. In addition, his lab is assessing the value of other imaging modalities such as OCT in the determination of optic nerve head changes that occur in early glaucoma.

Using a variety of in vivo and in vitro models of glaucoma, Morgan's group is investigating the mechanisms of retinal ganglion cell death in glaucoma. There is good evidence that these cells undergo a prolonged period of atrophy and remodeling prior to cell death, which is manifest as shrinkage and pruning in the cell body and dendritic processes. These changes will reduce the efficiency with which these cells can detect visual signals but also suggests that this damage could be reversed. They use techniques such as biolistics transfection to see if the overexpression of genes that might be beneficial for retinal neurons can result in cell rescue Retinal ganglion cell transfected with plasmid coding for GFP. Retinal Explant preparation after 24 hours in culture.