Corey Harwell

Harwell initially planned on pursuing a career in medicine, an early research experience in Cori Bargmann's laboratory led Harwell instead to the basic sciences and in particular to neurobiology.{{Cite web|last=|first=|date=August 26, 2019|title=Success Stories: Corey Harwell|url=https://www.ninds.nih.gov/About-NINDS/Workforce-Diversity/Success-Stories/Success-Stories-Corey-Harwell|url-status=live|archive-url=https://web.archive.org/web/20171005060052/https://www.ninds.nih.gov/About-NINDS/Workforce-Diversity/Success-Stories/Success-Stories-Corey-Harwell |archive-date=2017-10-05 |access-date=|website=NIH: NINDS}} As a graduate student, Harwell conducted his thesis research at the Massachusetts Institute of Technology under Elly Nedivi. He studied the role of the gene cpg15 (candidate plasticity gene 15) and its protein product in neural development and plasticity.{{Cite journal|last1=Putz|first1=Ulrich|last2=Harwell|first2=Corey|last3=Nedivi|first3=Elly|date=March 2005|title=Soluble CPG15 expressed during early development rescues cortical progenitors from apoptosis|journal=Nature Neuroscience|volume=8|issue=3|pages=322–331|doi=10.1038/nn1407|issn=1097-6256|pmc=3075944|pmid=15711540}}{{Cite journal|last1=Harwell|first1=Corey|last2=Burbach|first2=Barry|last3=Svoboda|first3=Karel|last4=Nedivi|first4=Elly|date=October 2005|title=Regulation of cpg15 expression during single whisker experience in the barrel cortex of adult mice|journal=Journal of Neurobiology|volume=65|issue=1|pages=85–96|doi=10.1002/neu.20176|issn=0022-3034|pmc=3062911|pmid=16010668}} Cpg15 had been found to be a target of intracellular signaling pathways important for synaptic plasticity.{{Cite journal|last1=Fujino|first1=Tadahiro|last2=Lee|first2=Wei-Chung Allen|last3=Nedivi|first3=Elly|date=November 2003|title=Regulation of cpg15 by signaling pathways that mediate synaptic plasticity|journal=Molecular and Cellular Neurosciences|volume=24|issue=3|pages=538–554|doi=10.1016/s1044-7431(03)00230-6|issn=1044-7431|pmc=3065975|pmid=14664806}} Increases in cpg15 expression caused changes in axon and dendrite growth, as well as synapse formation.{{Cite journal|last1=Nedivi|first1=E.|last2=Wu|first2=G. Y.|last3=Cline|first3=H. T.|date=1998-09-18|title=Promotion of dendritic growth by CPG15, an activity-induced signaling molecule|journal=Science|volume=281|issue=5384|pages=1863–1866|doi=10.1126/science.281.5384.1863|issn=0036-8075|pmc=3088013|pmid=9743502|bibcode=1998Sci...281.1863N}} Harwell and his colleague Ulrich Putz showed that expression of a soluble form of CPG15 promoted survival of cortical neuron progenitors in early brain development. Additionally, Harwell, with members of Karel Svoboda's group, demonstrated that cpg15 expression in adult mice could be diminished by sensory deprivation, raising the possibility that CPG15 functions in a neural activity-dependent manner.

After receiving his PhD, Harwell completed a postdoctoral fellowship in Arnold Kriegstein's laboratory at the University of California, San Francisco. There, Harwell investigated early neural development. He identified a role of the gene sonic hedgehog (shh) and its receptor, BOC1, in the formation of connections between layer II/III cortical neurons and their postsynaptic targets, the layer V corticalfugal neurons.{{Cite journal|last1=Harwell|first1=Corey C.|last2=Parker|first2=Philip R. L.|last3=Gee|first3=Steven M.|last4=Okada|first4=Ami|last5=McConnell|first5=Susan K.|last6=Kreitzer|first6=Anatol C.|last7=Kriegstein|first7=Arnold R.|date=2012-03-22|title=Sonic hedgehog expression in corticofugal projection neurons directs cortical microcircuit formation|journal=Neuron|volume=73|issue=6|pages=1116–1126|doi=10.1016/j.neuron.2012.02.009|issn=1097-4199|pmc=3551478|pmid=22445340}} Additionally, Harwell characterized the relationship between cell lineage and distribution of developing cortical interneuron circuits and found that cell lineage does not determine clustering of cortical interneurons{{Cite journal|last1=Harwell|first1=Corey C.|last2=Fuentealba|first2=Luis C.|last3=Gonzalez-Cerrillo|first3=Adrian|last4=Parker|first4=Phillip R. L.|last5=Gertz|first5=Caitlyn C.|last6=Mazzola|first6=Emanuele|last7=Garcia|first7=Miguel Turrero|last8=Alvarez-Buylla|first8=Arturo|last9=Cepko|first9=Constance L.|last10=Kriegstein|first10=Arnold R.|date=2015-09-02|title=Wide Dispersion and Diversity of Clonally Related Inhibitory Interneurons|journal=Neuron|volume=87|issue=5|pages=999–1007|doi=10.1016/j.neuron.2015.07.030|issn=1097-4199|pmc=4581718|pmid=26299474}}

Following his postdoctoral work, Harwell became an assistant professor at Harvard Medical School in the Department of Neurobiology. In 2021, his laboratory moved to the University of California, San Francisco. His laboratory continues to focus on neural development.{{Cite web|last=|first=|date=2020|title=Harwell Lab|url=https://www.harwelllab.hms.harvard.edu/|url-status=live|archive-url=https://web.archive.org/web/20180614132454/https://www.harwelllab.hms.harvard.edu/ |archive-date=2018-06-14 |access-date=|website=}}

The Harwell Lab investigates how the developmental origins and lineages of different neuron types affects their function in the adult brain. The lab approaches these questions using circuit tracing, molecular biology, and genetic tools in mice. Currently, the lab seeks to characterize the molecular diversity of neural progenitors and dissect the genetic and epigenetic programs that drive the differentiation of these progenitors and their assembly into functional neural circuits. Recently, the lab has uncovered important roles for glial cells in neural development as well.{{Cite journal|last1=Hill|first1=Steven A.|last2=Blaeser|first2=Andrew S.|last3=Coley|first3=Austin A.|last4=Xie|first4=Yajun|last5=Shepard|first5=Katherine A.|last6=Harwell|first6=Corey C.|last7=Gao|first7=Wen-Jun|last8=Garcia|first8=A. Denise R.|date=June 13, 2019|title=Sonic hedgehog signaling in astrocytes mediates cell type-specific synaptic organization|journal=eLife|volume=8|doi=10.7554/eLife.45545|issn=2050-084X|pmc=6629371|pmid=31194676 |doi-access=free }}{{Cite journal|last1=Baizabal|first1=José-Manuel|last2=Mistry|first2=Meeta|last3=García|first3=Miguel Turrero|last4=Gómez|first4=Nicolás|last5=Olukoya|first5=Olubusola|last6=Tran|first6=Diana|last7=Johnson|first7=Matthew B.|last8=Walsh|first8=Christopher A.|last9=Harwell|first9=Corey C.|date=July 11, 2018|title=The Epigenetic State of PRDM16-Regulated Enhancers in Radial Glia Controls Cortical Neuron Position|journal=Neuron|volume=99|issue=1|pages=239–241|doi=10.1016/j.neuron.2018.06.031|issn=1097-4199|pmid=30001508|doi-access=free}}

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