Jesse Cohn, PhD

Postdoctoral Research Fellow


Jesse grew up in Tulsa, OK and graduated from the University of Tulsa in 2008 with a degree in Biochemistry. In 2012, he began his Ph.D. work in the lab of Dr. Jon Pierce at the University of Texas-Austin, using C. elegans to investigate how long-term neural activity can affect several aspects of sensory neuron function. In the fall of 2019, Jesse joined the labs of Dr. Rob Mitra and Dr. Jeffrey Milbrandt to develop a novel high-throughput system for identifying genes, pathways, and principles involved in nervous system development.

Research Interest

Our current research project, dubbed “mChick,” uses the developing chick embryo as an in vivo development environment for mouse or human stem cells. By grafting these stem cells into the chick tissue of interest, they experience true developmental signals and morphogen gradients. This will allow the cells to follow more faithful developmental trajectories as compared to in vitro differentiation approaches. Furthermore, due to the complex morphogen gradients in developing tissue, this approach will give rise to a multitude of cell types in each experiment. When paired with single-cell sequencing techniques and CRISPRi/a libraries, we can probe questions related to cellular fate decisions in a parallel and efficient manner.

An area we intend to assess with this technique is the connection between mitochondrial metabolism and cell fate decisions. A pronounced shift in mitochondrial metabolism is known to occur during stem cell differentiation. This has been shown in several different stem cell types, such as hematopoietic stem cells, embryonic stem cells, and human induced pluripotent stem cells (hiPSCs). Importantly, this has also been demonstrated for neuronal precursor cells derived from hiPSCs. These experiments differentiated iPSCs in vitro using generic neuronal differentiation protocols, giving limited insight into the importance of this phenomenon for different types of neurons. Our “mChick” system would allow us to use CRISPR to reduce or increase expression of mitochondrial genes in implanted cells, which we could later analyze with regard to which cell types are present and to what degree they differentiated faithfully. In this way, we could probe this phenomenon in many different cell types at once, and in a physiologically relevant environment.

Mentor Jeffrey Milbrandt, MD, PhD and Rob Mitra, PhD