About the CRC 1064 Chromatin Dynamics
The SFB 1064 collaborative research center (CRC) Munich/Großhadern focuses on fundamental aspects of chromatin dynamics. It aims at understanding principles and mechanisms that endow chromatin organisation with diversity, flexibility and plasticity to respond to environmental and developmental cues. CRC research strives for an integrated understanding of chromatin structure and function from atomic resolution, via molecular interactions and mechanism to finally reach the microscopically resolvable structures of nuclei in physiological settings. It covers three major areas:
The role of energy-consuming nucleosome remodelling. We are interested in the structure and mechanism of nucleosome remodelling ATPases and the complexes they reside in, their roles in histone variant exchange, nucleosome positioning and nucleosome spacing as a prerequisite for faithful organisation of dynamic chromatin. A central question to address is how diverse remodelling machineries are targeted to specific loci, integrated into specific complexes, and regulated in the context of particular pathways.
Dynamics turnover of histone variants and modifications. This focus embraces all aspects of dynamic histone exchange, notably the exchange of canonical histones with structural variants and the cooperation of histone chaperones with remodelling machineries. The focus also deals with histone dynamics associated with the process of transcription through chromatin: We will better define the functional interactions between RNA polymerase and chromatin and attempt to gain insight into the structure of RNA polymerase II approaching a nucleosome.
Dynamic assembly and disassembly of chromatin structures. This focus addresses the dynamic aspects of chromatin organisation that were traditionally considered very stable, notably structures formed by classical heterochromatin proteins or Polycomb group (PcG) repressors, as well as dynamic reversal of DNA methylation. Several CRC projects are concerned with the reversal of tightly repressive structures, during the cell cycle, as part of the DNA damage response, or the reprogramming of cell identity during tissue regeneration and the activation of latent EBV epigenomes during the induction of the lytic phase.