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Faculty

  • Kim, Youngjo, Ph.D.

    Professor, Vice Director of SIMS

    Functional Genomics, Aging, Developmental Biology, Stem Cell Biology

    Room 306, SIMS

    +82-41-413-5023

    yjokim@sch.ac.kr

Our laboratory is interested in understanding how the nuclear lamina regulates cellular functions in development, homeostasis and aging. Lamins are the major structural components of the nuclear lamina that is associated with chromatin in the nucleus and connected to the cytoskeleton via nuclear membrane proteins. Since genetic mutations of lamins cause a list of human diseases such as premature aging, muscular dystrophy, and lipodystrophy, the study of lamins has taken a central stage not only in basic cell biology but also in clinical applications. Furthermore, recent studies show that physiological alteration of the nuclear lamina is involved in the development of age-associated tissue degeneration and metabolic disorders. Our research projects involve a wide range of experimental approaches, including genetics in model organisms, cell culture, biochemistry, and genomics.

 

Characterization of lamin-associated tissue dysfunctions

We have established various lamin knock out (KO) mice and mouse embryonic stem cells (mESC), including lamin-B1, -B2 and -A triple KO mESCs. Using various KO mouse and cell culture models, we are currently exploring the precise role of lamins in tissue functions and their implication in human diseases. We are also interested in examining the role of lamins in normal aging and development of metabolic disorders.

 

The mechanisms in which lamins regulate gene expression

Gene expression model is an attractive hypothesis to explain lamin-mediated tissue dysfunctions, which proposes that alteration of lamin expression or lamina structure causes changes in 3D genome organization and gene expression. We have shown the fundamental role of lamins in 3D genome organization using lamin TKO mESCs. Based on the principal acquired from mESCs, we will focus on elucidating the mechanism in which lamins regulate chromatin interactions and gene expression upon aging and metabolic imbalances.

 

Improvement of Hi-C technique and its application

Chromosome conformation capture (3C) technique and its derivatives such as Hi-C have provided high resolution 3D chromatin interaction maps and insights on genome organization and its function in gene expression. However, Hi-C analysis and other 3C-based techniques are limited to in vitro cultured cell lines mainly due to their requirements for massive amounts of samples. We are developing an efficient Hi-C technique that enables to map small number of cells, which might allow mapping 3D chromatin interactions from rare in vivo cell types.


Principal Investigator



Youngjo Kim, Ph.D.


Education

2001-2007, Ph.D. in Cell Biology, University of Georgia, Athens, GA, USA

1994-1996, M.S. in Biology, Sung Kyun Kwan University, Korea

1989-1993, B.S. in Biology, Sung Kyun Kwan University, Korea

 

Positions

2024-Present,  Professor, Soonchunhyang Institute of Medi-Bio Science (SIMS), Soonchunhyang University, Cheon-an, Korea

2018-2024, Associate Professor, Soonchunhyang Institute of Medi-Bio Science (SIMS), Soonchunhyang University, Cheon-an, Korea

2014-2018, Assistant Professor, Soonchunhyang Institute of Medi-Bio Science (SIMS), Soonchunhyang University, Cheon-an, Korea

2008-2014, Postdoctoral Associate, Carnegie Institution for Science, Baltimore, MD, USA

2007-2007, Postdoctoral Fellow, University of Georgia, Athens, GA, USA

1996-2001, Senior Research Scientist, Mogam Biotechnology Research Institute, Korea




Graduate Students


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Lidya Kristiani

Position: Doctoral candidate

Research interest: Development of Highly-Sensitive Hi-C Technique (HS-Hi-C)


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Miri Kim

Position: Doctoral candidate

Research interest: Investigating age-associated lamin B1 loss and kidney dysfunction in Drosophila and mouse model



Reni Marsela

Position: Master candidate

Research interest: Investigating 3D genome organization in lamin KO mouse models

 


Kristiani, L., Kim, M., and Kim, Y. (2020) Role of the nuclear lamina in age-associated nuclear reorganization and inflammation. Cells 9:718.

 

Kim, Y.*, Zheng X., and Zheng, Y. (2019) Role of lamins in 3D genome organization and global gene expression. Nucleus 10(1):33-41.

  

Zheng, X.#,*, Hu, J.#, Yue, S., Kristiani, L., Kim, M., Sauria, M., Taylor, J., Kim, Y.#,*, and Zheng, Y*. (2018) Lamins organize the global three-dimensional genome from the nuclear periphery. Mol Cell 71:802-815.

 

Kim, Y., Bayona, P.W., Kim, M., Chang, J., Hong, S., Park, Y., Budiman, A., Kim, Y.J., Choi, C.Y., Kim, W.S., Lee, J., and Cho, K.W. (2018) Macrophage lamin A/C regulates inflammation and the development of obesity-induced insulin resistance. Front Immunol 9:696.

  

Cho, K.W., Lee, J., and Kim, Y. (2016) Genetic variations leading to familial dilated cardiomyopathy. Mol Cells 39(10):722-727.

  

Zheng, X*., Kim, Y.*, and Zheng, Y. (2015) Identification of lamin B-regulated chromatin regions based on chromatin landscapes. Mol Biol Cell 26(8):2685-97.

  

Guo, Y., Kim, Y., Shimi, T., Goldman, R.D., and Zheng, Y. (2014) Concentration-dependent lamin assembly and its roles in the localization of other nuclear proteins. Mol Biol Cell 25(8):1287-97. 


Kim, Y. and Zheng, Y. (2013). Generation and characterization of a Conditional Deletion Allele for Lmna in Mice. Biochem Biophys Res Commun. 220(1):8-13.

  

Kim, Y., Zheng, X. and Zheng, Y. (2013). Proliferation and differentiation of mouse embryonic stem cells lacking all lamins. Cell Research 23(12):1420-3.

  

Kim, Y., McDole, K., and Zheng, Y. (2012). The function of lamins in the context of tissue building and maintenance. Nucleus 1;3(3): 256-62.

  

Kim, Y., Sharov, A.A., McDole, K., Cheng, M., Hao, H., Fan, C.M., Gaiano, N., Ko, M.S.H., and Zheng, Y. (2011). Mouse B-type lamins are required for proper organogenesis but not by embryonic stem cells. Science 334:1706-1710.

  

Bosu, D.R., Feng, H., Min, K., Kim, Y., Wallenfang, M.R. and Kipreos, E.T. (2010). C. elegans CAND-1 regulated cullin neddylation, cell proliferation and morphogenesis in specific tissues. Dev Biol. 346:113-126


Kim, Y., Starostina N.G. and Kipreos E.T. (2008). The CRL4Cdt2 ubiquitin ligase targets the degradation of p21Cip1 to control replication licensing. Genes Dev. 22:2507-2519.

  

Kim, Y. and Kipreos, E.T. (2007). Cdt1 degradation to prevent DNA re-replication: conserved and non- conserved pathways. Cell Div. 2:18.

  

Kim, Y. and Kipreos, E.T. (2007). The Caenorhabditis elegans replication licensing factor CDT-1 is targeted for degradation by the CUL-4/DDB-1 complex. Mol Cell Biol. 27:1394-406.