Objectives

Objectives and relevance of the joint research exchange programme
LCS addresses scientific issues related to “living cells study”. It is based on a 3 year joint programme of exchange of 18 staff members for periods ranging from 1 to 11 months, thus providing unique mobility possibilities to individual researchers and support to 3 research organizations to reinforce their long-term research co-operation.
The main aim of this project is to study chromatin dynamics during DNA repair, focusing our efforts on analysis of dynamics of chromatin-related proteins in living cells after induced DNA damage. Particularly to study dynamics of such proteins: HP1 (?, ?, ?), Jmjd2b (histone demetylase), BMI-1 (PcG-related protein), PML (Promyelocytic leukemia protein arranged into PML bodies).
The synergy of Czech expertise and the experience of Polish and Russian partners in these areas is a perfect match that will allow further advancements of science. Integration of the newest equipments and technologies together: 3D- confocal microscopy of living cells, FISH technique, immunohistochemistry, RT-PCR, Western blotting, ChIP-PCR, ChIP-onchips, FRAP, FLIP, FRET techniques (Czech and Polish partners) and Scanning Flow Cytometry (SFC), Fluorescence Microscopy (Russian partner) should give the good opportunity to reach the following objectives:
1. To study dynamics of chromatin-related proteins in living cells after induced DNA damage. Particularly to study dynamics of such proteins: HP1 (?, ?, ?), Jmjd2b (histone demetylase), BMI-1 (PcG protein), PML (PML body).
2. To study histone epigenetic changes, chromatin structure in relationship to gene expression in various cells types undergoing differentiation and to analyze on how chromatin structure is influenced by deficiency of histone methyltransferase Suv39h1. Moreover, importance of proteins (BMI-1), involved in Polycomb group protein complex (PRC1), will be studied from the view of nuclear architecture and gene expression.
3. Mouse fibroblasts with Suv39h deficiency will be treated by inhibitors of histone deacetylases such as trichostatin A (TSA) in order to induce hyperacetylation, which is expected to potentiate the effect of Suv39h deficiency on chromatin structure. Mechanisms of DNA reparation will be also addressed in Suv39h mouse experimental system in order to analyze an importance of histone signature during reparation of DSBs.

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