Yunji Seo

All Publications

• Successful Lymphatic Embolization for Genital Lymphorrhea in the Setting of Chronic Venous Insufficiency. Journal of vascular and interventional radiology : JVIR Seo, Y., Loening, A. M., Hung, M. L. 2026: 108845

  View details for DOI 10.1016/j.jvir.2026.108845

  View details for PubMedID 42107702

• Whole-genome 3D architectural screen reveals modulators of brain DNA structure. bioRxiv : the preprint server for biology Parasar, B., Venkatesh, A. R., Perera, J., Sosnick, L., Moghadami, S., Seo, Y., Shi, J., Chan, L., Takenawa, S., Akiyama, T., Sianto, O., Uenaka, T., Hadjipanayis, A., Wernig, M., Gitler, A. D., Tan, L. 2026

  Abstract

  Three-dimensional (3D) genome architecture is the foundation of gene regulation, and plays a critical role in normal physiology and disease. However, our understanding of its biochemical determinants has long been limited by technology: imaging-based screens only profile a small number of loci, while sequencing-based studies rarely exceed 100 samples or conditions. Here we present "in-plate chromosome conformation capture" (Plate-C), a high-throughput, cost-effective platform that profiles thousands of whole-genome architectures in a day. Plate-C enabled the first chemical screen for whole-genome structural changes-profiling 2,956 samples from 834 conditions across 5 neuronal and glial types, accompanied by 6,081 single cells using "easy diploid chromosome conformation capture" (Easy Dip-C) and 200,893 single-cell transcriptomes. We discovered that diverse, dose/time-dependent, and cell type/species-specific modes of DNA structural changes can be rapidly induced by manipulating epigenetic (HDAC, BET), metabolic (mTOR), proteostatic (UPR), developmental (GSK3/Wnt, Hedgehog), immune (cGAS/STING), and neurotransmission pathways. To validate our finding in vivo, we demonstrated in newborn mice that HDAC inhibition drives brain-wide genome rewiring within hours, highly correlated with changes in vitro and inducing a latent structural and transcriptional state orthogonal to normal differentiation. By enabling massively parallel profiling of whole-genome structures, Plate-C paves the way for systematic discovery of DNA folding principles to better understand and engineer the human genome in 3D.

  View details for DOI 10.64898/2026.04.15.718501

  View details for PubMedID 42039500

  View details for PubMedCentralID PMC13104906

• Whole-genome 3D architectural screen reveals modulators of brain DNA structure in vivo Venkatesh, A., Parasar, B., Sosnick, L., Moghadami, S., Seo, Y., Shi, J., Chan, L., Hadjipanayis, A., Tan, L. CELL PRESS. 2026

  View details for Web of Science ID 001717804800275

• GPNMB Biomarker Levels in GBA1 Carriers with Lewy Body Disorders. Movement disorders : official journal of the Movement Disorder Society Brody, E. M., Seo, Y., Suh, E., Amari, N., Hartstone, W. G., Skrinak, R. T., Zhang, H., Diaz-Ortiz, M. E., Weintraub, D., Tropea, T. F., Van Deerlin, V. M., Chen-Plotkin, A. S. 2024

  Abstract

  The GPNMB single-nucleotide polymorphism rs199347 and GBA1 variants both associate with Lewy body disorder (LBD) risk. GPNMB encodes glycoprotein nonmetastatic melanoma protein B (GPNMB), a biomarker for GBA1-associated Gaucher's disease.The aim of this study was to determine whether GPNMB levels (1) differ in LBD with and without GBA1 variants and (2) associate with rs199347 genotype.We quantified GPNMB levels in plasma and cerebrospinal fluid (CSF) from 124 individuals with LBD with one GBA1 variant (121 plasma, 14 CSF), 631 individuals with LBD without GBA1 variants (626 plasma, 41 CSF), 9 neurologically normal individuals with one GBA1 variant (plasma), and 2 individuals with two GBA1 variants (plasma). We tested for associations between GPNMB levels and rs199347 or GBA1 status.GPNMB levels associate with rs199347 genotype in plasma (P = 0.022) and CSF (P = 0.007), but not with GBA1 status.rs199347 is a protein quantitative trait locus for GPNMB. GPNMB levels are unaltered in individuals carrying one GBA1 variant. © 2024 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.

  View details for DOI 10.1002/mds.29773

  View details for PubMedID 38610104

• Lifelong restructuring of 3D genome architecture in cerebellar granule cells. Science (New York, N.Y.) Tan, L., Shi, J., Moghadami, S., Parasar, B., Wright, C. P., Seo, Y., Vallejo, K., Cobos, I., Duncan, L., Chen, R., Deisseroth, K. 2023; 381 (6662): 1112-1119

  Abstract

  The cerebellum contains most of the neurons in the human brain and exhibits distinctive modes of development and aging. In this work, by developing our single-cell three-dimensional (3D) genome assay-diploid chromosome conformation capture, or Dip-C-into population-scale (Pop-C) and virus-enriched (vDip-C) modes, we resolved the first 3D genome structures of single cerebellar cells, created life-spanning 3D genome atlases for both humans and mice, and jointly measured transcriptome and chromatin accessibility during development. We found that although the transcriptome and chromatin accessibility of cerebellar granule neurons mature in early postnatal life, 3D genome architecture gradually remodels throughout life, establishing ultra-long-range intrachromosomal contacts and specific interchromosomal contacts that are rarely seen in neurons. These results reveal unexpected evolutionarily conserved molecular processes that underlie distinctive features of neural development and aging across the mammalian life span.

  View details for DOI 10.1126/science.adh3253

  View details for PubMedID 37676945

• GPNMB confers risk for Parkinson's disease through interaction with alpha-synuclein SCIENCE Diaz-Ortiz, M. E., Seo, Y., Posavi, M., Cordon, M., Clark, E., Jain, N., Charan, R., Gallagher, M. D., Unger, T. L., Amari, N., Skrinak, R., Davila-Rivera, R., Brody, E. M., Han, N., Zack, R., Van Deerlin, V. M., Tropea, T. F., Luk, K. C., Lee, E. B., Weintraub, D., Chen-Plotkin, A. S. 2022; 377 (6608): 833-+

  Abstract

  Many risk loci for Parkinson's disease (PD) have been identified by genome-wide association studies (GWASs), but target genes and mechanisms remain largely unknown. We linked the GWAS-derived chromosome 7 locus (sentinel single-nucleotide polymorphism rs199347) to GPNMB through colocalization analyses of expression quantitative trait locus and PD risk signals, confirmed by allele-specific expression studies in the human brain. In cells, glycoprotein nonmetastatic melanoma protein B (GPNMB) coimmunoprecipitated and colocalized with α-synuclein (aSyn). In induced pluripotent stem cell-derived neurons, loss of GPNMB resulted in loss of ability to internalize aSyn fibrils and develop aSyn pathology. In 731 PD and 59 control biosamples, GPNMB was elevated in PD plasma, associating with disease severity. Thus, GPNMB represents a PD risk gene with potential for biomarker development and therapeutic targeting.

  View details for DOI 10.1126/science.abk0637

  View details for Web of Science ID 000843601300035

  View details for PubMedID 35981040