Dr. Nam-Sung MOON
Nam-Sung Moon completed his undergraduate and graduate studies at McGill University. For his Ph.D thesis, he investigated the mechanism of protein-DNA interaction of a transcription factor, CDP/Cut. He characterized the DNA binding property of CDP/Cut, which led to the identification of different CDP/Cut isoforms in cancer cells. To pursue his research interest in cell cycle regulation and cancer development, Dr. Moon joined the laboratory of Dr. Nick Dyson at Massachusetts General Hospital, Harvard Medical School. There, he investigated the function of RB/E2F family proteins using Drosophila as a model organism. Dr. Moon joined the Department of Biology at McGill as Assistant Professor in July 2008.
The Research in the Moon Lab
The balance between cellular division and programmed cell death (PCD) controls tissue sizes in metazoans. During organogenesis, cellular division contributes to mass increase, while PCD removes the surplus of cells that are potentially harmful to animals. Moreover, cellular division and PCD have to be tightly regulated during adulthood for proper homeostasis of a tissue. Failure to control these processes can often lead to development of disease such as cancer. The research goal of Dr. Moon is to investigate genes that are involved in cellular division and PCD using Drosophila melanogaster as a model organism.
Dr. Moon is particularly interested in understanding in vivo functions of the RB tumor suppressor gene. RB family proteins play an important role during G1 to S phase transition of the cell cycle. One of their key functions is to prevent abnormal S-phase entry by repressing E2F-dependent transcription. Timely expression of E2F target genes is necessary for proper S-phase entry. RB was the first identified tumor suppressor protein whose function is compromised in most cancer cells. As a consequence, cancer cells have deregulated E2F activity. Curiously, studies also have demonstrated that the loss of RB sensitizes cells to different apoptotic stimuli. Indeed, some E2F protein family members are potent inducers of cell death. The exact mechanism by which dE2F-dependent cell death is controlled during development, and how the cell death pressure generated by the loss of RB is suppressed in cancer cells are still unclear. In Dr. Moon laboratory, the Drosophila mutants of RB and E2F homologues are used to investigate these issues.
Morris EJ, Yuan JY, Yang F, Di Stefano L, Herr A, Moon NS, Kwon EJ, Haigis KM, Näär AM and Dyson NJ (2008) E2F1 represses β-catenin transcription and is antagonized by both pRB and CDK8. Nature. 455(7212):552-6
Moon NS, Di Stefano L, Morris EJ, Patel R, White K, and Dyson NJ (2008) E2F and p53 induce apoptosis independently during Drosophila development but intersect in the context of DNA damage. PLoS Genetics. 4(8):e1000153
Di Stefano L, Ji JY, Moon NS, Herr A, Dyson NJ (2007) Mutation of Drosophila Lsd1 disrupts H3-K4 methylation, resulting in tissue-specific defects during development. Current Biology. 7(9):808-12.
Morris EJ, Michaud WA, Ji JY, Moon NS, Rocco JW, Dyson NJ (2006) Functional identification of Api5 as a suppressor of E2F-dependent apoptosis in vivo. PLoS Genetics. 2(11):e196.
Moon NS, Di Stefano L, and Dyson NJ (2006) A gradient of EGFR signaling determines the sensitivity of rbf1 mutant cells to E2F-dependent apoptosis. Molecular and Cellular Biology. 26(20):7601-15
Moon NS, Frolov MV, Kwon EJ, Di Stefano L, Dimova DK, Morris EJ, Taylor-Harding B, White K, Dyson NJ (2005) Drosophila E2F1 has context-specific pro- and antiapoptotic properties during development. Developmental Cell. 9(4):463-75.
Stevaux O, Dimova DK, Ji JY, Moon NS, Frolov MV, Dyson NJ. (2005) Retinoblastoma family 2 is required in vivo for the tissue-specific repression of dE2F2 target genes. Cell Cycle. 4(9):1272-80.
Frolov MV*, Moon NS*, and Dyson NJ. (2005) dDP is required for normal cell proliferation. Molecular and Cellular Biology. 25(8):3027-39. (* Equal contribution)