Julia Lee-Soety, Ph.D.

Associate Professor
Disciplines Taught: Biology, Chemical Biology
Office: 227 Science Center
Phone: 610-660-3439
Fax: 610-660-1832
Email: jlee04@sju.edu

The ends of linear chromosomes in eukaryotic cells are protected by telomeres. The telomeric DNA interacts with many proteins including the telomerase enzyme complex that extends telomere ends and compensates for the end replication problem. Human stem and cancer cells express telomerase to facilitate immortality. Without telomerase however, telomeres shorten with each round of DNA replication; this gradual erosion eventually leads to cell senescence, an irreversible cell cycle arrest, and serves to control cellular life span. 
We are using baker’s yeast as model organism to study telomere dynamics. Yeast cells share several similar machineries as human cells, and insights we gain may be translated to understanding how telomeres contribute to cell aging and cancer biology.
Recently, yeast Npl3, a heterogeneous nuclear ribonucleoprotein-related protein have been attributed with telomere maintenance roles even though it is better known for processing RNA. When NPL3 is deleted in telomerase mutants, the rate of senescence is accelerated. Non-coding telomeric repeat containing-RNA (TERRA) levels are also significantly increased in these cells. TERRA molecules are transcribed from the seemingly silent subtelomeric region, and the expression and accumulation of TERRA have been shown to coincide with shortening of telomeres and cell senescence. How TERRA expression is correlated to cell senescence is not well understood. Because Npl3 interacts with proteins at multiple processes of gene expression, we are interested in understanding how Npl3 may be suppressing TERRA expression. By understanding how and where TERRA is regulated, we hope to further decipher how TERRA may stimulate cell senescence.


  • BS (1994) West Chester University, West Chester, PA
  • PhD (2002) University of Pennsylvania, Philadelphia, PA


Professional Experience

Post-doctoral Fellowship (2002-2006) Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine


Courses Taught

  • Biology I: Cells 
  • Wormy Genes
  • Immunology 
  • Molecular Genetics
  • Phage Genomics Lab



Lee-Soety, J.Y., J. Jones, M.A. MacGibeny, E.C. Remaly, L. Daniels, A. Ito, J. Jean, H. Radecki, and S. Spencer. 2012. Yeast hnRNP-related proteins contribute to the maintenance of telomeres. Biochem Biophys. Res. Comm. 426:12-17.

Lee*, J. Y., J. Mogen*, A. Chavez, and F. B. Johnson.  2008.  The Sgs1p RecQ helicase inhibits the survival of S. cerevisiae lacking telomerase and homologous recombination.  J. Biol. Chem. 283:29847-29858. * Authors contributed equally.

Hershman, S. G., Q. Chen, J. Y. Lee, M. A. Kozak, P. Yue, L.-S. Wang, and F. B. Johnson.  2008.  Genomic distribution and functional analyses of potential G-quadruplex-forming sequences in S. cerevisiae.  Nucl. Acids Res.  36:144-156.

Lee, J. Y., M. Kozak, J. D. Martin, E. Pennock, F. B. Johnson.  2007.  Evidence that a RecQ helicase slows senescence by resolving recombining telomeres.  PLoS Biology  5:1334-1344.

Azam*, M., J. Y. Lee*, V. Abraham, R. Chanoux, K. A. Schoenly, F. B. Johnson. 2006. Evidence that the S. cerevisiae Sgs1 protein facilitates recombinational repair of telomeres during senescence. Nucl. Acid Res. 34:506-516. * Authors contributed equally.

Lee, J. Y., N. Kim, A. Sanford, K. E. Sullivan. 2003. Histone acetylation and chromatin conformation are regulated separately at the TNFa promoter in monocytes and macrophages. J. Leuk. Biol. 73: 862-871.

Kilpatrick, L., J. Y. Lee, K. M. Haines, D. E. Campbell, K. E. Sullivan, and H. M. Korchak. 2002. Role for d-PKC and PI 3-kinase in TNFa mediated anti-apoptotic signaling in the human neutrophil. Am. J. Physiol. Cell Physiol. 283: C48-57.

Lee, J. Y.,D. Goldman, L. M. Piliero, M. Petri, K. E. Sullivan. 2001. Interferon-g polymorphisms in systemic lupus erythematosus. Genes Imm. 2: 254-257.

Lee, J. Y. and K. E. Sullivan. 2001. IFN-g modulation of LPS-inducible TNF-a expression occurs at the level of gene transcription. Infect. Imm., 69: 2847-2852.


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