Tenure in FRIS 2016.4-2021.5
|Research Fields||Epithelial cell biology, Developmental genetics, Developmental cell biology, Molecular biology|
|Academic Society Membership||Japanese Society for Developmental Biologists, The Molecular Biology Society of Japan, Genetics Society of America|
Epithelia are the foundation of organs and appendages throughout Metazoa and are a major source of human pathologies such as carcinomas. During embryogenesis and in adult, proliferating cells coordinate tissue growth or remodeling with morphogenesis to maintain their adhesive and polarized architecture. A tight balance of cell behaviors including cell division and death is particularly important for tissue homeostasis within the constraints of the epithelium. Although loss of tissue organization and alteration of cell fate have been assumed to be critical steps in epithelial pathogenesis, their causal relationship, underlying cellular dynamics and molecular networks are largely unknown.
My research interests are to understand how the polarized epithelial architecture is robustly maintained and to illuminate the causes of epithelial diseases by gaining mechanistic insights into the inherent plasticity of epithelial cells. Previously, I showed that the defects in mitotic spindle orientation in epithelia can trigger abnormal Epithelial-to-Mesenchymal Transition (EMT) and potential tumor formation (Figure). I am currently investigating mechanisms of aberrant cellular plasticity, or pathogenic cell-fates by studying EMT, tumorigenesis and regeneration using the Drosophila epithelia as a genetically tractable model. The overlapping objectives of my aims address a fundamental question: how does epithelial architecture maintain tissue homeostasis and suppress abnormal cell fate transformation? At the FRIS, I will introduce interdisciplinary approaches and elucidate the molecular and cellular machinery underlying biological phenomena.