Background
Mamalian
cells have two different repair pathways to repair DNA double strand
breaks:
- Non Homologous End Joining (NHEJ)
- Homologous Recombination Repair (HRR)
While
the first systems is active throughout the cell cycle, since it it
independent of a second copy of the damaged DNA, the latter one is
active only in late S and G2-Phase of the cell cycle. This reults in a
more error prone repair by NHEJ and a more accurate repair by HRR.
Our intrest is focussed on the late S and G2 phase, where both systems
are active.
How does a cell decide which repair system is used?
Can the pathways interact?
We study the interaction of repair proteins of these two pathways by
pairways analysis of severla members of these pathways following UV-A
exposure. Three techniques are used:
- optical colocalisation
- FRET measurements in fixed cells
- Co-immunoprecipitation in protein extracts
Recent results
Spatial interactions
We found
multiple interactions of the two repair pathways on different
levels. Including inter pathway interactions of NHEJ and HRR at
the same DSB site. The temporal sequence was found to include a first,
fast repair of DSBs by NHEJ and a subsequent repair by HRR at the same
site. Therefore a possible proofreading function of HRR can be assumed.
| DNA
Damage and Repair Topics |
|||
| UV-A
Induced DNA Damage |
DNA Repair Home |
Comet-assay
and Comet-FISH |
Intrinsic Oxidative
DNA Damages |