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Junichi Iwata, DDS, PhD

Dr. Junichi Iwata, DDS, PhD
  • Title: Associate Professor
  • Office: BBS-4208
  • Phone: 713-486-2641
  • Email:
  • Administrative Area(s): Diagnostic and Biomedical Sciences
  • Education:

    DDS | Kyushu University, Japan, 2000
    PhD | Kyushu University, Japan, 2004

Dr. Junichi Iwata is a tenured associate professor in the Department of Diagnostic and Biomedical Sciences at UTHealth School of Dentistry at Houston. 

The aim of his laboratory is to understand the cellular and molecular mechanisms in craniofacial birth defects and diseases such as cleft palate and xerostomia. Specifically, he is working to characterize the cell-signaling network and metabolism that directs craniofacial disorders, using multidisciplinary approaches including mouse genetics, genomics, proteomics, biochemistry, and molecular biology. The following research projects are ongoing in his laboratory:

Role of cellular metabolism during development and diseases

Cellular metabolic aberrations result in craniofacial deformities in humans and mice. The majority of cells in the craniofacial region are derived from cranial neural crest (CNC) cells, which is a multi-potent cell population that gives rise to a variety of different cell types. CNC cells are more sensitive to metabolic aberrations than those of other regions during embryogenesis. Dr. Iwata's team aims to identify gene mutations and protein modifications related to craniofacial disorders and provide the basis for tests aimed at identifying higher-risk persons.

Role of autophagic machinery in development and diseases

Autophagy is an evolutionarily conserved bulk-protein degradation system. This process is crucial for the removal and breakdown of cellular components such as damaged proteins and aged organelles. Autophagic activity is altered in various diseases and birth defects in humans and mice. An understanding of the manner in which autophagy is regulated is critical for understanding normal craniofacial development as well as congenital malformations. Dr. Iwata and his team are working to identify the molecular regulatory mechanism of autophagic machinery related to developmental defects and diseases.

Selected Publications:

1.    Suzuki A and Iwata J. (2014) Genetic and environmental risk factors for cleft lip and cleft palate. Progressive Science, 1: e01.


2.    Iwata J, Suzuki A, Yokota T, Ho TV, Pelikan R, Urata M, Sanchez-Lara P, and Chai Y. (2014) TGFß regulates epithelial–mesenchymal interactions via WNT signaling activity to control muscle development in the soft palate. Development, Feb; 141 (4): 909-17.


3.    Iwata J, Suzuki A, Pelikan RC, Ho TV, Sanchez-Lara PA, and Chai Y. (2014) Modulation of lipid metabolic defects rescues cleft palate in Tgfbr2 mutant mice. Hum. Mol. Genetics, Jan 1; 23 (1): 182-93.


4.    Iwata J, Suzuki A, Pelikan RC, Ho TV, and Chai Y. (2013) Cranial neural crest cells regulate tongue muscle formation via TGFß–mediated BMP and FGF signaling. J. Biol. Chem., 288: 29760-70.


5.    Song ZC*, Liu C*, Iwata J*, Gu SP, Suzuki A, Sun C, He W, Shu R, Li L, Chai Y, and Chen YP. (2013) Mice with Tak1-deficiency in neural crest lineage exhibit cleft palate associated with abnormal tongue development. J. Biol. Chem., Apr 12; 288 (15): 10440-50. (*These authors contributed equally to this work.)


6.    Iwata J, Suzuki A, Pelikan RC, Ho TV, Sanchez-Lara PA, Urata M, Dixon MJ, and Chai Y. (2013) Smad4Irf6 genetic interaction and TGFß–mediated IRF6 signaling cascade are crucial for palatal fusion in mice. Development, Mar; 140 (6): 1220-30.


7.    Pelikan RC*, Iwata J*, Suzuki A, Chai Y, and Hacia JG. (2013) Identification of candidate downstream targets of TGFß signaling during palate development by genome-wide transcript profiling. J. Cell Biochem., Apr, 114: 796-807. (*These authors contributed equally to this work.)


8.    Iwata J, Hacia JG, Suzuki A, Sanchez-Lara PA, Urata M, and Chai Y. (2012) Modulation of non-canonical TGF-ß signaling prevents cleft palate in Tgfbr2 mutant mice. J. Clin. Invest., Mar 1; 122 (3): 873-85.


9.    Iwata J, Tung L, Urata M, Hacia JG, Suzuki A, Ramenzoni L, Chaudhry O, Parada C, Sanchez-Lara PA, and Chai Y. (2012) Fibroblast growth factor 9 (FGF9)–pituitary homeobox 2 (PITX2) pathway mediates transforming growth factor beta (TGFß) signaling to regulate cell proliferation in palatal mesenchyme during mouse palatogenesis. J. Biol. Chem., Jan 20; 287 (4): 2353-63.


10.  Iwata J, Parada C, and Chai Y. (2011) The mechanism of TGF-ß signaling during palate formation: a novel target for prevention of cleft palate. Oral Diseases, Nov; 17 (8): 733-744.


11.  Iwata J, Hosokawa R, Sanchez-Lara PA, Urata M, Slavkin H, and Chai Y. (2010) Transforming growth factor-beta regulates basal transcriptional regulatory machinery to control cell proliferation and differentiation in cranial neural crest–derived osteoprogenitor cells. J. Biol. Chem., Feb 12; 285 (7): 4975-82.


12.  Sou Y*, Waguri S*, Iwata J*, Ueno T, Fujimura T, Hara T, Sawada N, Yamada A, Mizushima N, Uchiyama Y, Kominami E, Tanaka K, Komatsu M. (2008)  The Atg8 conjugation system is indispensable for proper development of autophagic isolation membranes in mice. Mol. Biol. Cell, 19 (11); 4762-75. (*These three authors contributed equally to this work.)


13.  Iwata J, Ezaki J, Komatsu M, Yokota S, Ueno T, Tanida I, Chiba T, Tanaka K, and Kominami E. (2006) Excess peroxisomes are degraded by autophagic machinery in mammals. J. Biol. Chem., 281, 4035-41.


Lab members:

Akiko Suzuki, DDS, PhD


Dhruvee Ramesh Sangani, DDS

Zhuofu Ni

Bahareh Ebadat

Pegah Ebadat