BEGIN:VCALENDAR
VERSION:2.0
PRODID:-//Memento EPFL//
BEGIN:VEVENT
SUMMARY:Novel Players in Chromatin
DTSTART:20141215T111500
DTSTAMP:20260510T020849Z
UID:e041205d831469ef5e093bd5979b230e8c0b3e0792bb75bb9ec0ec19
CATEGORIES:Conferences - Seminars
DESCRIPTION:Prof. Robert Schneider\, IGBMC\, Strasbourg (F)\nBIOENGINEERIN
 G SEMINARAbstract:\nOne of the major goals of post-genomic biological rese
 arch is to understand the molecular basis and physiological role of covale
 nt protein modifications. These post-translational modifications (PTMs) ca
 n regulate protein interactions and thus trigger particular downstream res
 ponses.  It has been suggested that PTMs of histones constitute a so-call
 ed "histone code" defining distinct chromatin or “epigenetic” states. 
 Nonetheless the set of characterised histone modifications is far from com
 plete and many modifications are awaiting identification.\nHow mechanistic
 ally chromatin and “epigenetic” states are inherited through cellular 
 divisions is currently only poorly understood. This inheritance of epigene
 tic states offers an important memory mechanism.  However to define the h
 eritability of epigenetic states within a population of cells is difficult
  due to cell heterogeneity\, combined with varying levels of stability of 
 these states. We are just beginning to understand how chromatin states (an
 d chromatin modulators) can mediate “epigenetic” memory and the inheri
 tance of these states on individual cell level.\nOne of the key questions 
 in the field is if histone PTMs can be causative for processes like transc
 ription or are just by-products\, with limited functional relevance. We re
 cently demonstrated a causative function for a novel lysine acetylation on
  the lateral surface of the histone octamer. We found that acetylations wi
 thin the core of the nucleosome at positions that are in contact with the 
 DNA are sufficient to stimulate transcription by modulating histone-DNA bi
 nding. Our model is that nucleosome function and signaling to the epigenom
 e is directly regulated by specific lateral surface modifications. Further
 more\, we identified additional novel PTMs that act as guardian of genome 
 stability by regulating the activity of transposable elements.Bio:\nRobert
  Schneider did his PhD at the LMU\, Munich (D)\, and was a postdoc at the 
 Gurdon Institute\, Cambridge\, UK. He then moved to the Max-Planck Institu
 te (MPI) of Immunobiology and Epigenetics\, Freiburg (D) and later from th
 ere to the IGBMC\, Strasbourg (F)\, where he leads the team ‘Functional 
 epigenetics and chromatin regulation’.
LOCATION:SV1717a http://map.epfl.ch/?room=sv1717a
STATUS:CONFIRMED
END:VEVENT
END:VCALENDAR
