My research focuses on the genetic basis and developmental mechanisms of congenital structural anomalies, particularly craniofacial developmental disorders, including cleft lip, cleft palate, frontonasal dysplasia, midfacial hypoplasia, micrognathia and missing or supernumerary teeth. We work to understand the causes and developmental mechanisms of congenital defects to improve diagnosis, treatment and patient care.
I majored in biology in college and actively conducted undergraduate research. I was fascinated by the processes of cell differentiation and received a master's degree in Genetics from the Chinese Academy of Science. Then I came to the United States for doctorate training in developmental biology.
Although my research projects during graduate and postdoctoral training mostly focused on uncovering basic cellular and molecular mechanisms of embryonic development, the results had clear applications in understanding pathogenic mechanisms of human developmental disorders. I decided to pursue an independent academic research career focused on understanding the genetic basis and developmental mechanisms of major structural birth defects.
More than 3 percent of children are born with developmental defects. Many of these children have defects in craniofacial structures that require surgical treatment shortly after birth. The causes and pathogenic mechanisms of most craniofacial congenital anomalies are not well understood. Our research aims to gain a comprehensive understanding of the cellular and molecular mechanisms of craniofacial development and provide solid scientific knowledge for the development and improvement of strategies for diagnosis, treatment and clinical care of children with such developmental disorders.
Some of my lab’s groundbreaking work include:
I am honored to have received many awards and appointments during my career, including:
I have been a researcher for more than 26 years and began working at Cincinnati Children's in 2011.
BS: Nanjing Normal University, Nanjing, China, 1984.
MS: Genetics, Chinese Academy of Sciences, Beijing, China, 1987.
PhD: Wesleyan University, Middletown, CT, 1995.
Genetic basis and developmental mechanisms of congenital craniofacial malformations; tendon development, homeostasis, and heterotopic ossification
Plastic Surgery, Developmental Biology
OSR1 disruption contributes to uterine factor infertility via impaired Müllerian duct development and endometrial receptivity. The Journal of Clinical Investigation. 2023; 133.
The transcription factors Foxf1 and Foxf2 integrate the SHH, HGF and TGFβ signaling pathways to drive tongue organogenesis. Development (Cambridge). 2022; 149.
Alx1 Deficient Mice Recapitulate Craniofacial Phenotype and Reveal Developmental Basis of ALX1-Related Frontonasal Dysplasia. Frontiers in Cell and Developmental Biology. 2022; 10:777887.
Mouse models in palate development and orofacial cleft research: Understanding the crucial role and regulation of epithelial integrity in facial and palate morphogenesis. Current Topics in Developmental Biology. 2022; 148:13-50.
The Scleraxis Transcription Factor Directly Regulates Multiple Distinct Molecular and Cellular Processes During Early Tendon Cell Differentiation. Frontiers in Cell and Developmental Biology. 2021; 9:654397.
Cis-Repression of Foxq1 Expression Affects Foxf2-Mediated Gene Expression in Palate Development. Frontiers in Cell and Developmental Biology. 2021; 9:665109.
Genome-wide Identification of Foxf2 Target Genes in Palate Development. Critical reviews in oral biology and medicine : an official publication of the American Association of Oral Biologists. 2020; 99:463-471.
Crucial and Overlapping Roles of Six1 and Six2 in Craniofacial Development. Critical reviews in oral biology and medicine : an official publication of the American Association of Oral Biologists. 2019; 98:572-579.
Mkx-Deficient Mice Exhibit Hedgehog Signaling-Dependent Ectopic Ossification in the Achilles Tendons. Journal of Bone and Mineral Research. 2019; 34:557-569.