CRC 1064: Chromatin dynamics
- Speaker: Professor Dr. Peter Becker
- Affiliation: Adolf Butenandt Institute
- Funding: since 2013
The SFB "Chromatin Dynamics" investigates basic principles of dynamic structural properties of chromatin, as well as mechanisms that determine the diversity and flexibility of chromatin and confer the necessary plasticity to react to signals of metabolism, the environment or in the course of development processes. In the SFB, complementary experimental approaches and concepts are intended to stimulate each other and contribute to the integrated view of chromatin organisation. The spectrum of view wraps ranges from the elucidation of structures with atomic resolution to the characterisation of multi-component complexes and the physiological structures of the cell nucleus, which can be resolved using advanced microscopy techniques. The focus is on the following areas: Nucleosomes Remodelling. The focus here is on the structure and function of complex nucleosome remodeling ATPases, their role in the positioning of nucleosomes, the exchange of histone variants and the construction of dynamic chromatins. It will be investigated how remodelling factors are recruited to their target sites in chromatin, integrated into specific complexes and regulated in a physiological context. Histone modifications and exchange of variants. This focus covers all aspects of the exchange of nucleosomal histones by variants and their incorporation by chaperones and remodellers. Equally interesting are the dynamic chromatin changes associated with the transcription of chromatin by RNA polymerase. Dynamics and resolution of repressive structures. The main structures of interest here are those that have traditionally been described as stable and stable, especially those that exhibit heterochromatin properties or are formed by Polycomb proteins. Some subprojects investigate the mechanisms by which such structures are resolved and altered, e.g. in the course of the cell cycle, DNA damage response, tissue regeneration and induction of the latent EBV genome during the lytic phase of infection.
Quelle: DFG Gepris