IFOM-KU Joint Research Laboratory

Makoto T. Hayashi Ph.D btn

Chromosomal abnormalities are directly linked to cell death and cell abnormalities, and contribute to the evolution of life in the long term. In particular, we are focusing on the functions of chromosome ends called telomeres. Using molecular genetic techniques that incorporate the latest genome editing and imaging techniques, we are aiming to understand tumorigenesis from the viewpoint of chromosome abnormalities. This laboratory is jointly established by the Graduate School of Medicine and the Institute of Molecular Oncology (IFOM: The FIRC Institute Molecular Oncology) Italy, and its research activities are conducted within our campus.

Research and Education

The end of the chromosome is protected from being recognized as DNA damage by a nucleoprotein complex called telomere. However, loss of telomere protection can lead to fusion of chromosomes (Fig. 1). Chromosome fusion is known to cause cell death, chromosome instability, and cancer depending on the cell type and environment, but it is not clear what conditions determine the cell fate after chromosome fusion. Therefore, our group has constructed a new cellular system (Fusion Visualization system: FuVis) that visualizes cells with a single defined chromosome fusion (Fig. 2). We are conducting daily research to understand the molecular mechanisms of various phenotypes caused by chromosome fusions.
There are master’s and doctoral students enrolled in this program, and each student is engaged in research on independent themes. Foreign students are also enrolled, and seminars are basically conducted in English. We have been certified as On-site Laboratory (Inbound type) and are actively conducting research exchanges as an international joint research laboratory. We welcome motivated students who are interested in basic research, so please feel free to email us for seeking details of our research.

Recent Publications

  1. V. Pragathi Masamsetti, Ronnie Ren Jie Low, Ka Sin Mak, Aisling O’Connor, Chris D. Riffkin, Noa Lamm, Laure Crabbe, Jan Karlseder, David C.S. Huang, Makoto T. Hayashi and Anthony J. Cesare: Replication stress induces mitotic death through parallel pathways regulated by WAPL and telomere deprotection. Nature Communications, 2019, September 17; 10(1): 4224
  2. Makoto T. Hayashi: Telomere biology in aging and cancer: early history and perspectives. Genes & Genetic Systems, 2017 Oct 6; 92, 107-118 doi: 10.1266
  3. Makoto T. Hayashi, Anthony J. Cesare, Teresa Rivera and Jan Karlseder: Cell Death During Crisis Is Mediated by Mitotic Telomere Deprotection. Nature, 2015, June 25; 522: 492-496
  4. Anthony J. Cesare, Makoto T. Hayashi, Laure Crabbe, and Jan Karlseder: The Telomere Deprotection Response Is Functionally Distinct from the Genomic DNA Damage Response. Molecular Cell, 2013, July 25; 51(2): 141-155
  5. Makoto T. Hayashi, Anthony J. Cesare, James A. J. Fitzpatrick, Eros Lazzerini-Denchi and Jan Karlseder: A Telomere Dependent DNA Damage Checkpoint Induced by Prolonged Mitotic Arrest. Nature Structural & Molecular Biology, 2012 Mar 11; 19(4): 387-394

IFOM-KU Joint Research Laboratory

Visiting Associate Professor: Makoto T. Hayashi, Ph.D

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075-753-9511 (Laboratory)
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