
Research Interests: Signaling control of mammalian morphogenesis and congenital disease
Our lab studies basic mechaniss by which signaling between cells coordinates mammalian morphogenesis. Understanding this control has significance beyond its fundamental importance in development since birth defects are the leading cause of death for infants during the first year of life. We utilize multiple approaches based in mouse genetics to understand fundamental signaling processes as they relate to development and disease with particular foci in the craniofacial and respiratory systems. In addition to mouse genetics approaches, we utilize human ES/IPSCs, biophysical approaches, multiomics, and live imaging to understand the cellular and molecular control of morphogenesis.
Publications
Eed controls craniofacial osteoblast differentiation and mesenchymal proliferation from the neural crest.
Alternative cleavage and polyadenylation of the Ccnb1 mRNA defines accumulation of cyclin protein during the meiotic cell cycle.
A Suite of Mouse Reagents for Studying Amelogenesis.
Exome sequencing efficacy and phenotypic expansions involving esophageal atresia/tracheoesophageal fistula plus.
A unique form of collective epithelial migration is crucial for tissue fusion in the secondary palate and can overcome loss of epithelial apoptosis.
Investigating Cell Fate Specification upon Nkx2-1Loss.
Tracheal separation is driven by NKX2-1-mediated repression of Efnb2 and regulation of endodermal cell sorting.
Cellular and molecular mechanisms of EPH/EPHRIN signaling in evolution and development.
Investigating the effects of compound paralogous EPHB receptor mutations on mouse facial development.
EPH/EPHRIN regulates cellular organization by actomyosin contractility effects on cell contacts.
Cellular and Molecular Regulation of Upper Lip Fusion.
Effects of EPHB receptors on facial morphology: non-additive interactions during mouse facial development.
Separation of the trachea and esophagus is coupled to identity specification by NKX2-1-mediated regulation of EPH/EPHRIN signaling and cell sorting.
YAP/TAZ Regulate Elevation and Bone Formation of the Mouse Secondary Palate.
Forced to communicate: Integration of mechanical and biochemical signaling in morphogenesis.
The UCSF Mouse Inventory Database Application, an Open Source Web App for Sharing Mutant Mice Within a Research Community.
Morphometric Analysis of Efnb1 Dependent Palate Growth.
Hypertelorism of Efnb1 Null Mice Occurs Independently of Changes to Underlying Brain Shape.
Cellular organization and boundary formation in craniofacial development.
WITHDRAWN: Editorial Introduction.
Editorial: Signaling pathways instruct the blueprint of life.
Getting direction(s): The Eph/ephrin signaling system in cell positioning.
Live Imaging of Mouse Secondary Palate Fusion.
Cellular dynamics of tissue fusion in craniofacial development and orofacial clefting.
EPHRIN-B1 Mosaicism Drives Cell Segregation in Craniofrontonasal Syndrome hiPSC-Derived Neuroepithelial Cells.
Unidirectional Eph/ephrin signaling creates a cortical actomyosin differential to drive cell segregation.
From Bench to Bedside and Back: Improving Diagnosis and Treatment of Craniofacial Malformations Utilizing Animal Models.
Neural crest defects in ephrin-B2 mutant mice are non-autonomous and originate from defects in the vasculature.
Convergence and extrusion are required for normal fusion of the mammalian secondary palate.
Embryonic expression of EphA receptor genes in mice supports their candidacy for involvement in cleft lip and palate.
Cell intercalation and migration mediated by actin contractility are key cellular behaviors in fusion of the mammalian secondary palate (344.2).
The society of craniofacial genetics and developmental biology 35th annual meeting.
The widely used Wnt1-Cre transgene causes developmental phenotypes by ectopic activation of Wnt signaling.
Ephrin B1 maintains apical adhesion of neural progenitors.
Palatogenesis: morphogenetic and molecular mechanisms of secondary palate development.
Eph/ephrin signaling: genetic, phosphoproteomic, and transcriptomic approaches.
Ephrin-B signaling in craniofacial development and disease.
Ephrin-B1 forward signaling regulates craniofacial morphogenesis by controlling cell proliferation across Eph-ephrin boundaries.
Analysis of signaling downstream of ephrin-B1 during development.
Ephrin-B1 regulates axon guidance by reverse signaling through a PDZ-dependent mechanism.
The TGF-beta pseudoreceptor gene Bambi is dispensable for mouse embryonic development and postnatal survival.
Inhibition of gap junction communication at ectopic Eph/ephrin boundaries underlies craniofrontonasal syndrome.
Development of the upper lip: Morphogenetic and molecular mechanisms.
Development of the upper lip: morphogenetic and molecular mechanisms.
Expression of Wnt9b and activation of canonical Wnt signaling during midfacial morphogenesis in mice.
The cleft lip and palate defects in Dancer mutant mice result from gain of function of the Tbx10 gene.
The T-box gene Tbx10 exhibits a uniquely restricted expression pattern during mouse embryogenesis.
Isolation and developmental expression analysis of Tbx22, the mouse homolog of the human X-linked cleft palate gene.
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