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SUMMARY:Chromatin modification blocks dedifferentiation of neurons to prev
 ent tumorigenesis - Abhijit Das (Gurdon Institute)
DTSTART:20160427T163000Z
DTEND:20160427T183000Z
UID:TALK65453@talks.cam.ac.uk
CONTACT:Clara Sidor
DESCRIPTION:Transition from self-renewing stem cells to differentiation is
  a key one-way process during development of an organism. Dedifferentiatio
 n of any cell type into its progenitor must be precisely blocked to preven
 t tumor formation. Studies using Drosophila neurogenesis as a model have i
 dentified key genes required for initiating the process of differentiation
  and waning stem-ness in differentiating neurons. Homeodomain transcriptio
 n factor Prospero plays a key role in restricting self-renewal in GMCs and
  initiating the process of differentiation (Choksi et al\, 2006). BTB-Zn f
 inger transcription factor Lola is required in neurons to prevent their de
 differentiation into neuroblasts (Southall et al\, 2014). However\, this t
 ype of developmental transition must be permanent and should accompany cha
 nges in chromatin conformation\, neither the nature or the mechanism of wh
 ich are well understood. I will discuss an epigenetic silencing mechanism 
 involving histone deacetylation and Su(var)3-9 mediated H3K9-trimethylatio
 n\, i.e. HP1 mediated heterochromatinization\, as the key mechanism for si
 lencing pluripotency genes and blocking the competence of self-renewal in 
 differentiating neurons\; removal of these components in newly born neuron
 s leads to dedifferentiation. A functional link between prospero & lola an
 d the heterochromatic silencing mechanism will also be discussed. 
LOCATION:Gurdon Institute Tea Room
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