Université de Strasbourg

Hajime Fukui


National Cerebral and Cardiovascular Center (NCVC), Osaka, Japan & USIAS Fellow at the Institute of Genetics and Molecular and Cellular Biology (IGBMC), University of Strasbourg

Hajime Fukui, USIAS Fellow 2017

Since 2012, Hajime Fukui is a staff scientist in the Department of Cell Biology at the National Cerebral and Cardiovascular Center (NCVC) Research Institute, Osaka, Japan. He obtained his PhD from Kyoto University (Laboratory of Bioimaging and Cell Signaling) in 2009. During his thesis, he detected a non-canonical function of seryl-tRNA synthetase (SerRS) that regulates vegfa transcription in vascular development. From 2009 to 2012, he was a tenured assistant professor at the Kyoto Prefectural University of Medicine (Department of Developmental Biology and Anatomy). He is interested in primary cilia signaling and focused on the ciliary proteins in the organ development. After moving to his current position, Hajime Fukui has identified the mechanisms by which the hippo signaling pathway regulates early cardiac development; S1P-Yap signaling requires cardiac precursor cell migration towards midline, and Lats1/2-Yap/Taz-dependent bmp2b transcription activation restricts cells in the second heart field.

During his research career, he has revealed part of the mechanisms of cardiac morphogenesis, utilizing zebrafish imaging and genetic approaches. His main objectives are to reveal the mechanism of cardiovascular development which is coordinately regulated by the genetically encoded signaling and force-driven signaling. He has received research grants from the Takeda Science foundation, SENSHIN-Medical Research Foundation, Uehara Memorial Foundation, Cell Science Research Foundation, and Grants-in-Aid for Scientific Research (from JSPS and MEXT) in Japan.


Project - Molecular mechanism of endocardial mechanotransduction during valvulogenesis

November 2017 - October 2019

Cardiovascular Diseases (CVDs) are the leading cause of death in the world. Heart malformations account for as many as 30% of embryos or fetuses lost before birth. On top of these statistics, another 2% of new-borns have bicuspid aortic valves (BAVs) or other valve defects, which may cause significant morbidity and mortality later in life. Congenital heart valve malformations, therefore, constitute an important medical issue challenging our society.

The zebrafish is one of the most widely used animal models for developmental and regeneration studies. Among its advantages is its relatively small size (2-4 cm), which enables several hundreds or thousands of animals to be housed in a small to medium-sized, cost-effective facility. Adults give rise to large numbers of embryos, which can be maintained completely translucent for up to 5 days post-fertilization, by which time organogenesis is complete.

Formation of the cardiac valve is orchestrated by genetically-encoded several signaling and mechanical stimulation generated by intracardial flow via expression of krüppel-like factor 2 (klf2). In zebrafish, Notch and Wnt activation in endocardial cells are influenced by a cardiac contraction and/or blood flow, highlighting an essential link between mechanical stimuli and developmental gene networks. However, the identity of the mechanosensory pathway directly activated by intracardial flow during valve formation remains unclear.

We aim to identify the mechanosensory pathway and to reveal the molecular mechanisms of mechanotransduction involved in the process of valvulogenesis. To accomplish this goal, we will determine the identity of the mechanosensors that are responsible for valvulogenesis and characterize the role of the uncovered mechanosensory pathway.


  • Web page of the Department of Cell Biology at the National Cerebral and Cardiovascular Center (NCVC) Research Institute, Osaka, Japan
  • Article in eLife : Hippo signaling determines the number of venous pole cells that originate from the anterior lateral plate mesoderm in zebrafish (eLife 2018;7:e29106 doi: 10.7554/eLife.29106)
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