Chromatin modification blocks dedifferentiation of neurons to prevent tumorigenesis

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• Abhijit Das (Gurdon Institute)
• Wednesday 27 April 2016, 17:30-19:30
• Gurdon Institute Tea Room.

If you have a question about this talk, please contact Clara Sidor.

Transition from self-renewing stem cells to differentiation is a key one-way process during development of an organism. Dedifferentiation of any cell type into its progenitor must be precisely blocked to prevent tumor formation. Studies using Drosophila neurogenesis as a model have identified key genes required for initiating the process of differentiation and waning stem-ness in differentiating neurons. Homeodomain transcription factor Prospero plays a key role in restricting self-renewal in GMCs and initiating the process of differentiation (Choksi et al, 2006). BTB -Zn finger transcription factor Lola is required in neurons to prevent their dedifferentiation into neuroblasts (Southall et al, 2014). However, this type of developmental transition must be permanent and should accompany changes in chromatin conformation, neither the nature or the mechanism of which are well understood. I will discuss an epigenetic silencing mechanism involving histone deacetylation and Su(var)3-9 mediated H3K9 -trimethylation, i.e. HP1 mediated heterochromatinization, as the key mechanism for silencing pluripotency genes and blocking the competence of self-renewal in differentiating neurons; removal of these components in newly born neurons leads to dedifferentiation. A functional link between prospero & lola and the heterochromatic silencing mechanism will also be discussed.

This talk is part of the Cambridge Fly Meetings series.

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