Dr. Kato is a tenureed scientist who is conducting research on the molecular mechanism of vertebrate development. He teaches Microbiology at the medical school and Bioregulation at the graduate school.
Dr. Kato is a native of Japan, where he obtained his medical degree in 1992 from Nagoya City University Medical School. He went on to obtain a Ph.D. in biochemistry, and moved to the U.S. in 1997 to pursue a research fellowship at Boston Children's Hospital/Harvard Medical School.
M.D. - Nagoya City University Medical School, Japan, 1986-1992
Resident - Department of Internal Medicine, Nagoya City University Hospital, 1992-1993
Ph.D. - Department of Biochemistry, Nagoya City University Medical School, Japan, 1993-1997
Research Fellow - Department of Neurology, Boston Children's Hospital/Harvard Medical School, 1997-2003
FSU University Service
Voting member, Animal Care and Use Committee (2009–2011).
FSU Department Service
Member, Faculty Evaluation Committee (2013-
member, Physician Assistant Program committee (2014-
member, Space Committee (2014-
Member, Faculty recruitment committee (2011–2012).
Member, Core Facility Committee (2010–2011).
Member, Faculty Search Committee (2008).
Member, Graduate School administration committee (2006–2008).
Member, Faculty Search Committee (2005).
Member, Faculty Development Committee (2005–2006).
Member, Promotion and Tenure Committee (2004–2005).
1997-1997 Fellowship of Japan Society for the Promotion of Science
2000-2001 Fellowship of Uehara Memorial Foundation
2001-2003 Fellowship of The Medical Foundation
Society for Development Biology
Society for Neuroscience
We focus on dissecting the role of signal trunsduction pathways during development. In my lab, two major projects are going on:
1) Ciliogenesis during development
The cilium is a small cellular organelle which broadly exists throughout the human body in either motile or immotile form. Motile cilia generate force by beating for directional fluid movement, whereas primary (non-motile) cilia are involved in sensory processes and cellular signaling. Disruption of ciliary structure and/or function in humans causes pleiotropic disorders, called ciliopathies. Although a certain length of motile cilia is important for their normal function, the molecular mechanism that regulates cilia length still remains to be explored. We recently found that blocking the Smad2/3-dependent TGF-ß (Xnr1 and Derrière) pathway in Xenopus embryos shortened motile cilia in several tissues. We further found that the role of TGF-ß signaling seems to be independent of known mechanisms that regulate cilia formation including ciliary length control. However, the mechanism that is regulated by TGF-ß signaling still remains unknown. To understand the mechanism of ciliary length control, we will analyze this mechanism by using state-of-art technologies such as next generation sequencing and proteomics.
2) Identifying chemical compounds that regulate neuronal differentiation
Stem cell therapy holds considerable promise for the treatment of degenerative diseases. Stem cells are differentiated into required cell types to replace non-functional tissues in degenerative diseases and injuries to functional normal tissues. Stem cell differentiation is regulated by both intrinsic regulators and the extracellular environment, and can be controlled ex vivo by cell culture manipulation with ‘‘cocktails’’ of growth factors, signaling molecules, and/or by genetic manipulation. A challenge to disseminate stem cell therapy is to establish inexpensive and safe methods by which stem cells are differentiated into required cell types. However, purified growth factors are still expensive, and risk of genetic manipulation to recipients with transplantation of these cells is also considerable. Since human or mouse embryonic stem cells have been hampered by multiple technical challenges, we are using Xenopus embryos for high-throughput screening (HTS) of chemical compound libraries to identify new chemical compounds. We have identified some compounds to control neuronal differentiation.
Tözser J, Earwood R, Kato A, Brown J, Tanaka K, Didier R, Megraw T, Blum M, Kato Y. (2015). Activation of TGF-ß signaling is required to control the length of motile cilia. Cell Rep, 11, 1-8.
Manojlovic Z, Earwood R, Kato A, Stefanovic B, Kato Y. (1014).RFX7 is required for the formation of cilia in the neural tube. Mech Dev, 32, 28-37.
Tanaka K, Kato A, Angelocci C, Watanabe M, Kato Y. (2014).A potential molecular pathogenesis of cardiac/laterality defects in Oculo-Facio-Cardio-Dental syndrome. Dev Biol, 387, 28-36.
Xu Y, Xu C, Kato A, Tempel W, Abreu JG, Bian C, Hu Y, Hu D, Zhao B, Cerovina T, Diao J, Wu F, He HH, Cui Q, Clark E, Ma C, Barbara A, Veenstra GJ, Xu G, Kaiser UB, Liu XS, Sugrue SP, He X, Min J, Kato Y, Shi YG. (2012). Tet3 CXXC Domain and Dioxygenase Activity Cooperatively Regulate Key Genes for Xenopus Eye and Neural Development. Cell, 151, 1200-13.
Kato, Y. (2011). The multiple roles of Notch signaling during left-right patterning. Cell Mol Life Sci, 68(15), 2555-67.
Sakano, D., Kato, A., Parikh, N., McKnight, K., Terry, D., Stefanovic, B., & Kato, Y. (2010). BCL6 Canalizes Notch-Dependent Transcription, Excluding Mastermind-like1 from Selected Target Genes during Left-Right Patterning. Dev Cell, 18(3), 450-462.
Koide, Y., Kiyota, T., Tonganunt, M., Pinkaew, D., Liu, Z., Kato, Y., Hutadilok-Towatana, N., Phongdara, A., & Fujise, K. (2009). Embryonic lethality of fortilin-null mutant mice by BMP-pathway overactivation. Biochimica Et Biophysica Acta-General Subjects, 1790(5), 326-338.
Kiyota, T., Kato, A., Altmann, C. R., & Kato, Y. (2008). The POU homeobox protein Oct-1 regulates radial glia formation downstream of Notch signaling. Dev Biol, 315(2), 579-592.
Kiyota, T., Kato, A., & Kato, Y. (2007). Ets-1 regulates radial glia formation during vertebrate embryogenesis. Organogenesis, 3(2), 93-101.
Zhang, W., Chen, X., Kato, Y., Evans, P. M., Yuan, S., Yang, J., Rychahou, P. G., Yang, V. W., He, X., Evers, B. M., & et al. (2006). Novel cross talk of Kruppel-like factor 4 and beta-catenin regulates normal intestinal homeostasis and tumor repression. Mol Cell Biol, 26, 2055-2064.
Nakaya, M., Habas, R., Biris, K., Dunty, W., Kato, Y., He, X., & Yamaguchi, T. (2004). Identification and comparative expression analyses of Daam genes in mouse and Xenopus. Gene Expr Patterns, 1, 97-105.
Kato Y, Shi Y, He X. “Neuralization of the Xenopus embryo by inhibition of p300/ CREB-binding protein function.” J Neurosci, 1999,19, 9364-73.
Kato Y, Habas R, Katsuyama Y, Naar A, He X. “A component of the ARC/Mediator complex required for TGF-beta/Nodal signaling.” Nature, 2002, 418, 641-46.
Zhang W, Chen X, Kato Y, Evans PM, Yuan S, Yang J, Rychahou PJ, Yang VW,He X, Evers BM, Liu C. Novel Cross Talk of Kruppel-Like Factor 4 and ?-Catenin Regulates Normal Intestinal Homeostasis and Tumor Repression. Mol Cell Biol. 2006; 26: 2055-64.
Kiyota T, Kato A, Kato Y. Ets-1 regulates radial glia formation during vertebrate embryogenesis. Organogenesis 2007, 3: 93-101.
Kiyota T, Kato A, Altmann CR, Kato Y. The POU homeobox protein Oct-1 regulates radial glia differentiation downstream of Notch signaling. Developmental Biology 2008, 315: 579-592.
Koide Y, Kiyota T, Tonganunt M, Tonganunt M, Pinkaew D, Liu Z,Kato Y, Towantana N, Phongdara A, FujiseK. Embryonic Lethality of Fortilin-null mutant mice by BMP-pathway overactivation. BBA 2009, 1790: 326-338.
Sakano D, Kato A, Parikh N, McKnight K, Terry D, Stefanovic B and Kato Y. BCL6 canalizes Notch-dependent transcription, excluding Mastermind-like1 from selected target genes during left-right patterning. Developmental Cell 2010, 18: 450–462.