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Saturday, November 24, 2012
BCL6 controls neurogenesis through Sirt1-dependent epigenetic repression of selective Notch targets
During neurogenesis, neural stem/progenitor cells (NPCs)
undergo an irreversible fate transition to become neurons. The Notch
pathway is important for this process, and repression of Notch-dependent
Hes genes is essential for triggering differentiation. However,
Notch signaling often remains active throughout neuronal
differentiation, implying a change in the transcriptional responsiveness
to Notch during the neurogenic transition. We identified Bcl6,
an oncogene, as encoding a proneurogenic factor that is required for
proper neurogenesis of the mouse cerebral cortex. BCL6 promoted the
neurogenic conversion by switching the composition of Notch-dependent
transcriptional complexes at the Hes5 promoter. BCL6 triggered exclusion of the co-activator Mastermind-like 1 and recruitment of the NAD+-dependent deacetylase Sirt1, which was required for BCL6-dependent neurogenesis. The resulting epigenetic silencing of Hes5
led to neuronal differentiation despite active Notch signaling. Our
findings suggest a role for BCL6 in neurogenesis and uncover
Notch-BCL6-Sirt1 interactions that may affect other aspects of
physiology and disease.
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