Julia Lee-Soety, Ph.D.
Chromosome ends (or telomeres) shorten over time in many human cells; this shortening plays a role in controlling cellular life span, thus the natural processes of aging. On the other hand, the inappropriate relengthening of telomeres is involved in cancer cell survival. It is crucial for cells to preserve proper telomere function and to maintain the ends of chromosomes. My lab is interested in understanding how two RNA-processing proteins may be involved in telomere maintenance. We are using baker’s yeast as the model organism. Baker’s yeast are eukaryotic cells that have many similarities to human cells including ways in which proteins work. Because we are able to conduct various experiments in yeast that we cannot easily do in human cells, the insight we gain in the yeast system will further the understanding of telomere biology in human.
Nucleolin and heterogenious nuclear ribonucleoprotein (hnRNP A1) in human cells are important in rRNA maturation and maturation, ribosome assembly, and nucleoplasmic transport. Recently these proteins have been found to be involved in maintaining telomeres since they interact directly with telomeric DNA. The yeast Nsr1p is homologous to human nucleolin, and Npl3 is homologous to hnRNP A1. We have shown that these proteins, when deleted in yeast cells that mimic aging human cells, caused the cells to be even more sick. We have designed experiments to explore mechanisms of how Nsr1p and Npl3p work at yeast telomeres. These protein contain several very interesting protein domains that we want to examine further and explore how they contribute to the functions of the proteins. Studying the dynamics of telomeres, how they are maintained, and their regulation by various factors has and will continue to add to the understanding of the natural processes of aging and cancer.
- BS (1994) West Chester University, West Chester, PA
- PhD (2002) University of Pennsylvania, Philadelphia, PA
Post-doctoral Fellowship (2002-2006) Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine
- Biology I: Cells (Fall)
- Immunology (Fall)
- Molecular Genetics (Spring)
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.