The establishment of distinct cell fates is a prerequisite for the development of complex multicellular organisms. A striking paradigm for this diversification can be observed in the vascular endothelium, which differentiates to form arterial, venous, lymphatic and organ specific networks. Current dogma suggests that following specification from mesoderm, environmental cues define the molecular and functional characteristics of endothelial cells in different vascular beds. I will present evidence to challenge this view, showing that lymphatic endothelial fate is imprinted as cells transition through a subset of mesoderm, a finding with broad implications for our understanding of cell lineage commitment.
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I am currently a British Heart Foundation Transition Research Fellow in the Department of Physiology, Anatomy and Genetics at the University of Oxford. My research harnesses zebrafish and rodent models to understand the cellular and molecular mechanisms controlling cardiovascular development and disease. I obtained my PhD from the University of Bristol and then trained in the laboratory of Didier Stainier at the Universtiy of California, San Francisco and Max Planck Institute for Heart and Lung Research. My work has identified the earliest known transcriptional regulator of endothelial cell differentiation (Reischauer*, Stone* et al., Nature, 2016), established a link between metabolic dysfunction and innate immune signalling in endothelial cells (Stone et al., Nature Comms, In Press), and is currently focused on defining the cellular and molecular events that determine endothelial cell fate and heterogeneity.