Karthik Shekhar, PhD

Assistant Professor

About Dr. Shekhar

Karthik Shekhar is an Assistant Professor of Chemical and Biomolecular Engineering at UC Berkeley, where he started his research group in 2020. He obtained his undergraduate degree in chemical engineering at the Indian Institute of Technology, Bombay; PhD in chemical engineering at MIT. During his postdoc, he switched his interests to neuroscience, and led some of the early efforts applying single-cell genomic approaches to study neural diversity at the Broad Institute of MIT and Harvard. His current research aims to understand the development and evolution of cell types in the visual system, particularly the retina. He has been a recipient of the NIH Pathway to Independence Award, the Hellmann Foundation fellowship, and is a fellow of the Glaucoma Research Foundation.

Research Areas

The development of neural diversity

The visual system is an accessible microcosm of the brain, and contains a staggering array of diverse neuronal types differing in morphology, function and molecular profile. By combining single-cell genomic measurements and statistical inference approaches, we study how this neural diversity is shaped during early development. We are interested in both experience-dependent and experience-independent contributions to the sculpting of neural diversity.

The evolution of neural diversity

The retina, located at the back of the eye, is the neural tissue where visual processing begins. The basic blueprint of the retina is shared by all vertebrates, yet different species, from jawed fish to rodents to primates, profoundly differ in their visual needs. One might expect that retinal cell types would vary in accordance with these needs, but this has not been systematically studied. Using single-cell genomic profiles, we hope to systematically assess the conservation of cell types across species to gain insight into the evolution of neural diversity. Through this analysis, we hope to identify non-primate counterparts of the major primate cell types, whose loss underlies the pathogenesis of blinding diseases.