Yoshihiro Komatsu, Ph.D.
- Assistant Professor
- Graduate School
- Kumamoto University, Kumamoto, Japan, 2004
- University of Michigan, Ann Arbor, MI, 2009-2012
Areas of Interests
Our research interests are in the genetic and molecular mechanisms that orchestrate embryonic development. Our lab focuses on two fields: ciliopathies and craniofacial skeletal defects. We found that bone morphogenetic protein (BMP) signaling regulates the transient formation of cilia at the node, the critical component required to establish the left-right asymmetry. We also found that augmentation of BMP signaling altered the skeletogenic cell fate in neural crest cells that leads to skull shape abnormalities. Our study will identify the previously uncharacterized molecular mechanisms that will allow for the development of new therapeutic directions for birth defects and craniofacial bone-related treatment.
Noda K, Shiozawa Y, Komatsu Y. Molecular etiology of craniosynostosis. Genet Disord Gene Ther. 2013, 1: 101.
Komatsu Y, Yu PB, Kamiya N, Fukuda T, Ray MK, Yamamura KI, Mishina Y. Augmentation of Smad-dependent BMP signaling in neural crest cells causes craniosynostosis in mice. Journal of Bone and Mineral Research. 2013, 28, 1422-1433.
Komatsu Y, Mishina Y. Establishment of left-right asymmetry in vertebrate development: the node in mouse embryos. Cellular and Molecular Life Sciences. 2013, 70, 4659-4666.
Komatsu Y, Kaartinen V, Mishina Y. Cell cycle arrest in node cells governs ciliogenesis at the node to break left-right symmetry. Development. 2011, 138, 3915-3920.
Komatsu Y, Scott G, Nagy A, Kaartinen V. Mishina Y. BMP type I receptor ALK2 is essential for proper patterning at late gastrulation during mouse embryogenesis. Developmental Dynamics. 2007, 236, 512-517.