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Yoichi Kato M.D., Ph.D.

Yoichi Kato M.D., Ph.D.

Associate Professor

yoichi.kato@med.fsu.edu
(850) 645-1481
Main Campus

Job Description


Dr. Kato is a tenured 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.

CURRENTLY ACCEPTING NEW GRADUATE STUDENTS.

Biosketch

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.

Education


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

Service


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).

Honors/Awards


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

Memberships

Society for Development Biology
Society for Neuroscience

Research Focus

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.

Publications


Manojlovic Z, Earwood R, Kato A, Perez D, Cabrera OA, Didier R, Megraw TL, Stefanovic B, Kato Y.(2017). La-Related protein 6 controls ciliated cell differentiation. Cilia, 6, 4.

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. (2014). 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.