Home ＞GCOE Researchers ＞Kunihiro MATSUMOTO

GCOE Researchers

Kunihiro MATSUMOTO

Affiliation
/Position		 Graduate School of Science, Division of Biological Science, Professor
Doctorate Doctor of Engineering
Research interests Molecular genetics, Signal transduction mechanisms
address g44177a＠nucc.cc.nagoya-u.ac.jp
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+81-52-789-3000
  Laboratory

Outline of research

The organization of the vertebrate body plan is based on a “blueprint” written in the DNA. This plan is implemented by temporally and spatially inducing cell responses in response to various signal molecules. The signal transduction networks in which these molecules act govern development, differentiation and the nervous system. Therefore, understanding these networks is an important step in elucidating the mechanisms by which the vertebrate body plan is generated. We discovered and analyzed TAK1, a novel member of the MAP kinase cascade, and then characterized the signal transduction pathway regulated by TAK1 cascade as well as its role in development and differentiation. In the process, we cultivated many young researchers and created new research horizons. Currently, we are identifying novel signal transduction factors and are analyzing their functions in development, differentiation, and the nervous system.

  1. Signal transduction network regulated by the TAK1 cascade: Using our uniquely developed molecular genetic techniques, we identified TAK1, a signal transduction factor in a novel MAP kinase cascade in mammals. We demonstrated that the TAK1 cascade functions in the TGF- pathway, that cell fate determination in early embryonic development is regulated by cross-talk of the TAK1 cascade with the Wnt signaling pathway, and further that the TAK1 cascade functions as a key factor in the control of inflammation and cell death.
  2. Signal transduction network at the level of the organism: Using C. elegans and Drosophila as model animals, we revealed p38-type and JNK-type MAP kinase signal pathways that regulate development, differentiation and the nervous system at the level of the whole organism. Furthermore, we have constructed knockout C. elegans strains that lack the signal transduction factors that control the MAP kinase cascade, and established a pioneering system that allows analyses of the MAP kinase cascade network at the organism level.
  3. Establishment of a model system for genetic diseases, using C. elegans as a model animal: In the course of research on signal transduction pathways in C. elegans, it was revealed that newly identified signal transduction factors genes are also involved in genetic diseases such as Alzheimer's and Parkinson's. We demonstrated the mechanism of action of these genes in C. elegans. Understanding the function of the signal transduction pathway in C. elegans allowed us to establish a model system for the study of genetic diseases.

References

  1. Hanafusa H. et al. (2008) Regulation of the ERK activity duration by Sprouty contributes to dorsoventral patterning. Nat. Cell Biol., In press.
  2. Olahova M. et al. (2008) A redox-sensitive peroxiredoxin that is important for longevity has tissue- and stress-specific roles in stress resistance. Proc. Natl. Acad. Sci. USA, In press.
  3. Mizuno T. et al. (2008) Role of the C. elegans Shc adaptor 1 protein in the JNK signaling pathway. Mol. Cell. Biol., In press.
  4. Hisamoto N. et al. (2008) C. elegans WNK-STE20 pathway regulates tube formation by modulating ClC channel activity. EMBO Rep., 9: 70-75.
  5. Kim J.Y. et al. (2008) TAK1 is a central mediator of NOD2 signaling in epidermal cells. J. Biol. Chem., 283: 137-144.
  6. Omori E. et al. (2008) TAK1 regulates reactive oxygen species and cell death in keratinocytes, which is essential for skin integrity. J. Biol. Chem., 283: 26161-26168.
  7. Takada1 I. et al. (2007) A histone lysine methyltransferase activated by non-canonical Wnt signalling suppresses PPAR-γtransactivation. Nat. Cell Biol., 9: 1273-1285.
  8. Sakaguchi-Nakashima A. et al. (2007) LRK-1, a C. elegans PARK8-related kinase, regulates axonal-dendritic polarity of SV proteins. Curr. Biol., 17: 592-598.
  9. Orsborn A.M. et al. (2007) GLH-1, the C. elegans P granule protein, is controlled by the JNK KGB-1 and the COP9 subunit CSN-5. Development, 134: 3383-3392.
  10. Kajino T. et al. (2007) TAK1 MAPKKK mediates TGF-βsignaling by targeting SnoN oncoprotein for degradation. J. Biol. Chem., 282: 9475-9481.

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