Tokyo Institute of Technology Department of Bioscience and Biotechnology
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 STAFF Professor : Shigehisa HIROSE,
Assistant Prof. : Akira KATO,  Nobuhiro NAKAMURA
 
Website of the HIROSE Lab. >>  http://www.evolution.bio.titech.ac.jp/index_e.html

 

  Research
Our mission at Hirose Laboratory is to clarify the mechanisms of intercellular communication and the formation of such communication networks at the molecular level. In particular, our research has focused on receptors acting in the circulatory system. Recently, we have been examining complex biological systems, using animals adapted to extreme conditions, for our better understanding of chemistry of life and for establishing molecular bases for future biotechnology.
1. Mechanism of maintaining body fluid homeostasis
(1)@Molecular biology of chloride cells or ionocytes
Little is understood about how aquatic creatures live when there is a significant difference in the degree of osmotic pressure between that within their bodies and that of the sea or fresh water they inhabit. This mystery is one of the major challenges for biology in the 21st century. We are attempting to solve this riddle by taking a molecular biology approach to looking at ionocytes which play a primary role in the regulation of osmotic pressure.  
(2)@Genetic approach using animal models
Using the blowfish and zebrafish (for both of which the genome is being mapped), we are aiming to utilise genetic analysis to understand the homeostatic mechanism of the circulatory system.  
2. Receptor processing and intracellular traffic
(1)@Hirose Laboratory discovered and named Ig-Hepta, a receptor which has a unique structure and processing mechanism. We are now analysing its physiological role by generating a KO mouse, a totally unexpected role important in the medical field.  
(2)@We have discovered a new family of proteins which control intracellular traffic and the shape of mitochondria and we are in the process of clarifying the underlying mechanisms.  
3. S‘Ÿ‚ΖΤŒŒ‹…‚Μ”­Ά§Œδ
(1)@We are clarifying the mechanisms of differentiation of early cardiomyocytes and parallel alignment of myofibrils using a zebrafish mutant, which has a defect in a connexin gene, cx36.7.  
(2)@Identification of cis and trans factors and clarification of the mechanism of heart-specific expression of cx36.7.  

Recent publications

1) Sultana,N.et al.(2008)Zebrafish early cardiac connexin, Cx36.7/Ecx, regulates myofibril orientation and heart morphogenesis by establishing Nkx2.5 expression.Proc. Natl. Acad. Sci. USA.. 105, 4763-4768.
2) Nakamura,N.et al.(2008)Regulation of Mitochondrial Morphology by USP30, a deubiquitinating enzyme present in the mitochondrial outer Membrane.Mol.Biol.Cell 19,
1903-1911.
3) Esaki,M.et al.(2007)Visualization of Na+ uptake in mitochondrion-rich cells whose differentiation is dependent on foxi3a. in zebrafish larvae.Am. J. Physiol. 292 (1), R470-R480.

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