Shan Meltzer is a neuroscientist and Assistant Professor in the Department of Pharmacology at Vanderbilt University School of Medicine. Meltzer's research focuses on the developmental principles of sensory neurons and the role of signaling pathways in sensory development. ^[1] By using an integrative approach that combines mouse genetics, anatomical studies, physiological analysis, and behavioral research, Meltzer's work explores the key molecular and cellular mechanisms underlying somatosensory circuit assembly. These efforts have significant potential in understanding and treating nerve injuries, chronic pain, and somatosensory dysfunctions linked to various diseases ^[2].

Shan Meltzer pursued her undergraduate studies at Peking University, where she earned bachelor's degrees in Life Sciences and Philosophy. Following her undergraduate education, she joined the Neuroscience graduate program at University of California, San Francisco (UCSF) in 2012, where she worked under the mentorship of Yuh Nung Jan.

During her graduate studies, Meltzer focused on the development and function of Drosophila sensory neurons. Her research unveiled the role of dendrite-extracellular matrix (ECM) adhesion in sensory dendrite patterning. Her research revealed that mutations in the semaphorin ligand Sema-2b disrupt dendrite-ECM adhesion, leading to excessive dendrite self-crossing and a failure to confine dendrites to a two-dimensional plane. This work, published in Neuron (2016), significantly advanced the understanding of dendrite self-avoidance mechanisms.^[3]

Meltzer also unveiled the critical role of phosphatidylethanolamine (PE) synthesis pathways in sensory neurons, which support dendrite growth and function. This study demonstrated how phospholipid homeostasis regulates dendrite morphogenesis in sensory neurons.^[4]

After completing her graduate studies, Meltzer received postdoctoral training in the Department of Neurobiology at Harvard Medical School, in the lab of David Ginty. During this time, she pioneered research in understanding the molecular and cellular mechanisms of mammalian somatosensory circuit assembly, authoring multiple research articles. Her postdoctoral work focused on the developmental steps and molecular pathways that regulate the precision formation of touch sensory neurons (Meltzer et al., 2021).^[5]

In a published study on gamma-Protocadherins, Meltzer investigated the roles of clustered protocadherin gamma (Pcdhg) isoforms in the development of touch sensory neurons. The Pcdhgc3 isoform plays a key role in promoting synapse formation between sensory neurons and spinal cord neurons. Loss of Pcdhg isoforms disrupts sensory input to the spinal cord, impairing the assembly of spinal cord circuitry and reducing corticospinal synapses on dorsal horn neurons (Meltzer et al., 2023). ^[6]

In another published study, Meltzer investigated the roles of axon-glial interactions and Netrin-G1 signaling in the formation of low-threshold mechanoreceptors (LTMRs) in the formation of sensory end organs. Experimental findings, including the ablation of Ntng1 (Netrin-G1) and Lrrc4c (NGL-1), demonstrated that disrupting these signaling pathways can impair the formation of lanceolate complexes, a key component of hair follicle-associated LTMRs and other mechanoreceptor end organs (Meltzer et al., 2022).^[7]

Meltzer’s research contributes to the understanding of sensory neuron development and the molecular mechanisms underlying sensory processing. Her work continues to advance knowledge in the field of sensory neuroscience and may inform future studies in this area. After completing the postdoctoral phase of her fellowship, Meltzer transitioned to a faculty position as an assistant professor at Vanderbilt University School of Medicine, where she continues her research on somatosensory circuit development.^[8]

Meltzer is a recipient of the Howard Hughes Medical Institute Hanna H. Grey Fellowship, which supports her postdoctoral work as well as her independent research.^[9]

• 2025 C.J. Herrick Award in Neuroanatomy, American Association for Anatomy ^[10]
• 2023 MIT Biology Catalyst Fellow, Massachusetts Institute of Technology^[11]
• 2023 Intersections Science Fellows Symposium Fellows^[12]
• 2019 Harvard Brain Science Initiative Young Scientist Travel Award^[13]
• 2016 Chancellor’s Diversity Award for the Advancement of Women, UCSF^[14]

• Kuehn, E.D.*, Meltzer, S.*, Abraira V.E., Ho C., and Ginty D.D. (2019). Tiling and Somatotopic Alignment of Mammalian Low-Threshold Mechanoreceptors. Proceedings of the National Academy of Sciences 116, 9168–9177. (*co-first authors) https://www.pnas.org/doi/10.1073/pnas.1901378116 ^[6]
• Meltzer, S., Comeau, K., Chirila, A., Osei-Asante, E., DeLisle, M., Zhang, Q., Kalish, B.T., Tasnim, A., Huey, E., Fuller, L.C., Flaherty, E.K., Lefebvre, J.L., Maniatis, T., Garrett, A.M., Weiner, J.A., and Ginty, D.D. (2023). γ-Protocadherins Control Synapse Formation and Peripheral Branching of Touch Sensory Neurons. Neuron 111, 1-19. https://www.cell.com/neuron/fulltext/S0896-6273(23)00208-8^[15]
• Meltzer, S., Boulanger, K. C., Osei-Asante, E., Handler, A., Zhang, Q., Sano, C., Itohara, S., and Ginty, D. D. (2022). A role for axon–glial interactions and Netrin-G1 signaling in the formation of low-threshold mechanoreceptor end organs. Proceedings of the National Academy of Sciences 119(43), e2210421119. https://www.pnas.org/doi/abs/10.1073/pnas.2210421119 ^[7]
• Meltzer, S., Santiago, C., Sharma, N., and Ginty, D.D. (2021). The Cellular and Molecular Basis of Somatosensory Neuron Development. Neuron 109, 1–22. https://linkinghub.elsevier.com/retrieve/pii/S0896-6273(21)00658-9 ^[5]
• Meltzer, S., Bagley, J.A., Perez, G.L., O’Brien, C.E., DeVault, L., Guo, Y., Jan, L.Y., and Jan, Y.N. (2017). Phospholipid Homeostasis Regulates Dendrite Morphogenesis in Drosophila Sensory Neurons. Cell Reports 21, 859–866. https://linkinghub.elsevier.com/retrieve/pii/S2211-1247(17)31409-2 ^[4]
• Meltzer, S., Yadav, S., Lee, J., Soba, P., Younger, S.H., Jin, P., Zhang, W., Parrish, J., Jan, L.Y., and Jan, Y.N. (2016). Epidermis-Derived Semaphorin Promotes Dendrite Self-Avoidance by Regulating Dendrite-Substrate Adhesion in Drosophila Sensory Neurons. Neuron 89, 741–755. https://linkinghub.elsevier.com/retrieve/pii/S0896-6273(16)00045-3 ^[3]