The goal of our research program is to uncover the mechanisms that direct a retinal progenitor cell (RPC) to exit the cell cycle and differentiate as an individual retinal neurons or glia. Neuronal diversity in the retina (>120 cell types in mice) is achieved through a temporal progression of RPCs through competence states, whereby the RPCs both gain and lose the ability to generate cell types as development progresses.

Current areas of focus seek to understand 1) DNA methylation status is dynamically controlled to facilitate neuronal diversity in post-mitotic cells; 2) How cis-regulatory sequence activity controls temporally dynamic gene expression independent of changes in chromatin accessibility; 3) Identify temporally dynamic long non-coding RNAs as putative regulators of retinal gene regulatory networks and retinal development; 4) Computational predictions of novel cell fate regulators in the developing retina; 5) Characterization of the dynamic changes in retinal epigenetics underlying retinal aging; 6) Identify novel genetics of inherited retinal disease and to understand the cellular mechanisms whereby pathogenic variants are causative of retinal degeneration.

By understanding the molecular basis of retinal development, we seek to inform treatment strategies to promote retinal regeneration or cellular replacement strategies for the treatment and cure of retinal disease. 

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As progress - socially, economically, and scientifically - is enhanced by input from diverse perspectives, experiences, and backgrounds, the Clark lab is committed to providing an inclusive training environment for all, regardless of one's identity/beliefs/background. Together, as an inclusive entity, we strive for progress in both science and beyond.