Junichi Iwata
Professor
The University of Texas Health Science Center at Houston
School of Dentistry
Department of Diagnostic and Biomedical Sciences
The aim of our laboratory is to understand the cellular and molecular mechanisms in craniofacial birth defects and diseases such as cleft lip and palate, tooth developmental defects, bone diseases, muscle disorders, and Sjögren’s syndrome. Specifically, we are working to characterize the cell-signaling network and cellular metabolic processes related to membrane trafficking, using multidisciplinary approaches—including genetics, genomics, proteomics, bioinformatics, biochemistry, and molecular biology. The following research projects are ongoing in our laboratory:
Research Projects:
Role of cellular metabolism in development and diseases
Cellular metabolic aberrations (including abnormal cholesterol metabolism) result in craniofacial deformities in humans and mice. Interestingly, mice with cholesterol synthesis deficiency have severe malformations specifically in the craniofacial region. Because the majority of cells in the craniofacial region stem from cranial neural crest (CNC) cells—which is a multi-potent cell population that gives rise to a variety of different cell types—we conclude that CNC cells are more sensitive to cellular metabolic aberrations than are cells from other regions during embryogenesis. However, the mechanism behind how molecules related to cellular metabolism are regulated during craniofacial development is still unknown. In addition, the possible relationship between cellular metabolism and craniofacial deformities remain unclear. The aim of our laboratory is 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, in which isolation membranes engulf cytoplasmic constituents and the resulting autophagosomes transport them to lysosomes. This process is critical for the removal and breakdown of cellular components such as damaged proteins and aged organelles. Because autophagic activity is altered in various diseases and birth defects in humans and mice, an understanding of the way autophagy is regulated is critical for understanding both normal craniofacial development and congenital malformations. The aim of our laboratory is to identify the molecular regulatory mechanism of autophagic machinery related to developmental defects and diseases.
Molecular regulatory mechanism of calvarial bone development and homeostasis
Craniofacial skeletal defects are one of the most prominent genetic disorders. However, the etiology of these defects remains largely unclear. This study will provide a new insight into cholesterol metabolism in craniofacial skeletal development, and will have a significant impact on the therapeutics of various types of bone diseases.
Role of WNT signaling in muscle development and regeneration
Various mutations in genes and proteins involved in signal transduction cause muscle abnormalities in both humans and mice. This study will provide insights into muscular disorders caused by mutations in genes involved in WNT/β-catenin signaling pathway. The results of this work will facilitate an understanding of how altered WNT/β-catenin signaling results in defects in muscle development and regeneration.
Transcripts and functions targeted by non-coding RNAs in lip and palate development
The etiology of cleft lip with/without cleft palate is complicated with a variety of genetic and environmental factors. This study will identify the distribution and contribution of non-coding RNAs (ncRNAs) in lip and palate development. The results of this study will facilitate our understanding of the role of ncRNAs in lip and palate development and will enable us to design future therapeutic approaches to diagnose and prevent cleft lip with/without cleft palate.
Education & Training
DDS, Kyushu University, 2000
PhD, Kyushu University, 2004