Nathan Harris

Dr. Harris received his PhD in Neuroscience from the University of California San Francisco in 2018 under the mentorship of Dr. Grae Davis. Dr. Harris identified a pathway of innate immune molecules that regulate synaptic vesicle release and a form of presynaptic homeostatic plasticity at the Drosophila melanogaster neuromuscular junction. He then moved to Brandeis University for his postdoc where he was advised by Dr. Piali Sengupta. He established single neuron gene expression profiling in C. elegans thermosensory neurons, enabling discovery of experience-dependent regulatory mechanisms that modulate neuronal function and behavior.

Research Interests
Every neuron needs to decide which of its tens of thousands of genes to express and how much of each gene product to make. As an animal navigates the world, these neuronal gene expression decisions are continually updated based on the environment. We aim to understand how an animal’s experience alters the gene expression profiles of its neurons, and how these gene expression responses generate plasticity.
To address this question, we use an ideal model system – sensory neurons of the nematode C. elegans. This system has a number of advantages: 1) These neurons can be activated by quantitatively controlled, ecologically relevant environmental stimuli; 2) C. elegans sensory circuits drive well characterized behaviors and behavioral plasticity; 3) Individual C. elegans neurons are identifiable and invariant from one animal to the next, meaning we can do experiments at true single neuron resolution; 4) We can predict, manipulate, and causally test the functions of individual gene regulatory elements, such as transcription factor binding sites, in a fully intact and behaving worm.
We rely heavily on RNA sequencing, CRISPR-Cas9, and high resolution imaging.