Novel Players in Chromatin
Event details
| Date | 15.12.2014 |
| Hour | 11:15 |
| Speaker | Prof. Robert Schneider, IGBMC, Strasbourg (F) |
| Location | |
| Category | Conferences - Seminars |
BIOENGINEERING SEMINAR
Abstract:
One of the major goals of post-genomic biological research is to understand the molecular basis and physiological role of covalent protein modifications. These post-translational modifications (PTMs) can regulate protein interactions and thus trigger particular downstream responses. It has been suggested that PTMs of histones constitute a so-called "histone code" defining distinct chromatin or “epigenetic” states. Nonetheless the set of characterised histone modifications is far from complete and many modifications are awaiting identification.
How mechanistically chromatin and “epigenetic” states are inherited through cellular divisions is currently only poorly understood. This inheritance of epigenetic states offers an important memory mechanism. However to define the heritability 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 (and chromatin modulators) can mediate “epigenetic” memory and the inheritance of these states on individual cell level.
One of the key questions in the field is if histone PTMs can be causative for processes like transcription or are just by-products, with limited functional relevance. We recently demonstrated a causative function for a novel lysine acetylation on the lateral surface of the histone octamer. We found that acetylations within the core of the nucleosome at positions that are in contact with the DNA are sufficient to stimulate transcription by modulating histone-DNA binding. Our model is that nucleosome function and signaling to the epigenome is directly regulated by specific lateral surface modifications. Furthermore, we identified additional novel PTMs that act as guardian of genome stability by regulating the activity of transposable elements.
Bio:
Robert 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 Institute (MPI) of Immunobiology and Epigenetics, Freiburg (D) and later from there to the IGBMC, Strasbourg (F), where he leads the team ‘Functional epigenetics and chromatin regulation’.
Abstract:
One of the major goals of post-genomic biological research is to understand the molecular basis and physiological role of covalent protein modifications. These post-translational modifications (PTMs) can regulate protein interactions and thus trigger particular downstream responses. It has been suggested that PTMs of histones constitute a so-called "histone code" defining distinct chromatin or “epigenetic” states. Nonetheless the set of characterised histone modifications is far from complete and many modifications are awaiting identification.
How mechanistically chromatin and “epigenetic” states are inherited through cellular divisions is currently only poorly understood. This inheritance of epigenetic states offers an important memory mechanism. However to define the heritability 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 (and chromatin modulators) can mediate “epigenetic” memory and the inheritance of these states on individual cell level.
One of the key questions in the field is if histone PTMs can be causative for processes like transcription or are just by-products, with limited functional relevance. We recently demonstrated a causative function for a novel lysine acetylation on the lateral surface of the histone octamer. We found that acetylations within the core of the nucleosome at positions that are in contact with the DNA are sufficient to stimulate transcription by modulating histone-DNA binding. Our model is that nucleosome function and signaling to the epigenome is directly regulated by specific lateral surface modifications. Furthermore, we identified additional novel PTMs that act as guardian of genome stability by regulating the activity of transposable elements.
Bio:
Robert 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 Institute (MPI) of Immunobiology and Epigenetics, Freiburg (D) and later from there to the IGBMC, Strasbourg (F), where he leads the team ‘Functional epigenetics and chromatin regulation’.
Practical information
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