Current Projects

Using N-ethyl-N-nitrosourea mutagenesis and phenotype-based genetic screening in mice combined with whole exome sequencing, we have identified a mutation in the Golgb1 gene as the cause of cleft palate in one mutant mouse line. Golgb1 encodes a ubiquitously expressed Golgi-associated protein involved intracellular vesicle trafficking. Understanding how loss of function of Golgb1 disrupts palate morphogenesis will provide unique insights into the cellular and molecular mechanisms of palate development. In addition, we are collaborating with the laboratory of Dr. Rulang Jiang in the elucidation of the molecular network consisting of major signaling pathways and transcription factors in the regulation of palate development.
We previously showed that the Osr2 transcription factor suppresses Msx1-mediated propagation of mesenchymal odontogenic potential during tooth development. Using a combination of laser capture microdissection, RNA-seq, and compound mutant mouse studies, we aim to identify the downstream targets and molecular pathways mediating Msx1 and Osr2 function in the regulation of tooth induction and morphogenesis.
We collaborate with other craniofacial research labs and clinicians in the Cincinnati Children’s Hospital Craniofacial Center to identify potential causal genetic variants in children born with craniofacial malformations using whole exome sequencing and functional studies of the candidate genes using CRISPR/Cas9-mediated genome editing in cell and/or animal models.
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