MassIVE MSV000090946

Partial Public PXD039041

Ovol2 sustains postnatal thymic epithelial cell identity

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Description

Thymic epithelial cells (TECs) begin to develop embryonically in mice and humans, expand in number through puberty, and then stabilize before declining during early adulthood. We identified a mechanism by which TEC numbers and function are maintained postnatally, discovered through a forward genetic screen for altered immune cell development in mice. A viable missense allele (C120Y) of Ovol2 resulted in lymphopenia, in which T cell development was compromised by loss of medullary TECs and dysfunction of cortical TECs. OVOL2 is an essential regulator of epithelial to mesenchymal transition (EMT), and we show that the epithelial identity of TECs is subverted towards a mesenchymal state in OVOL2-deficient mice. We document global changes in chromatin accessibility correlated with gene expression, particularly affecting genes involved in epithelial and mesenchymal cell proliferation and differentiation. OVOL2 regulates chromatin accessibility by inhibiting the BRAF-HDAC complex. In particular, it disrupts the RCOR1-LSD1 complex by directly binding to the lysine demethylase LSD1, resulting in inhibition of LSD1-mediated H3K4me2 demethylation. Thus, OVOL2 controls the epigenetic landscape of TECs, preventing EMT and enforcing TEC identity to support T cell development in the thymus. [doi:10.25345/C5H98ZJ5G] [dataset license: CC0 1.0 Universal (CC0 1.0)]

Keywords: OVOL2, TECs, thymus, LSD1/RCOR1 complex

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Principal Investigators:
(in alphabetical order) 		Jin Huk Choi, University of Texas Southwestern Medical Center, USA
Submitting User: JJMoresco
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