Dr. Markus Räschle, Project Leader

Tel.: +49 (0)631-205-5919
Fax: +49 (0)631-205-4090
Email: markus.raeschle[at]bio.uni-kl.de
Room: 24-101A

Project description:

Our group uses cutting-edge mass spectrometry to study DNA repair processes. We comprehensively monitor the assembly of DNA repair complexes on chromatin as it undergoes replication and repair in Xenopus egg extracts. From the proteomic profiles we identify novel factors with potential roles in DNA repair and the maintenance of genome stability. Using a variety of biochemical and cell biological assays we try to pinpoint their precise function during the repair process.
Over the past years this approach has reveal several new genome stability factors with important functions in the repair of psoralen crosslinks. By covering additional DNA repair pathways we aim at obtaining a system-wide view of DNA repair.

Dr. Maja Kneißig, Postdoctoral Student

Tel.: +49 (0)631-205-5920
Fax: +49 (0)631-205-4090
Email:kneissig[at]bio.uni-kl.de
Room: 24-109

Project description:

Genomic aberrations in cancer cells are thought to arise through a gradual process of mutation and selection. However, recent progress in genomic sequencing technologies has enable the discovery of a radically different phenomenon of genetic instability termed chromotripsis. In this case, massive shattering and random reassembly of single chromosome and/or chromosome regions lead to the formation of highly derivative chromosomes within one cell cycle. What initiates the chromosome damage, and which processes are involved in the repair of the DNA breaks remain unknown. The focus of my study is to understand the cellular and molecular mechanisms of chromotripsis in human cells.

Dr. Galal Metwally, Postdoctoral Student

Tel.: +49 (0)631-205-5920
Fax: +49 (0)631-205-4090
Email: gmetwa[at]bio.uni-kl.de
Room: 24-109 

Project Description:

http://www.uni-kl.de/aktuelles/news/news/detail/News/humboldt-stipendiat-erforscht-einfluss-von-veraenderter-chromosomen-anzahl-auf-den-zellzyklus/

Dr. Maria Krivega, Postdoctoral Student

Tel. +49 (0)631-205-5919
Fax: +49 (0)631-205-4090
Email: krivega[at]rhrk.uni-kl.de
Room: 24-101

Project description:

Although human cells can partially tolerate aneuploidy, the presence of an extra chromosome deregulates several physiological pathways and causes proteotoxic stress due to imbalanced protein expression. One of the key changes is upregulation of autophagy, which is a pathway that enables cells to dispose of unnecessary or dysfunctional components. In our group, we aim to uncover the upstream signaling pathways required for autophagy activation and to identify the components that are cleared by autophagy from aneuploid cells.

Paul Menges - PhD Student

Tel.: +49 (0)631-205-5919
Fax: +49 (0)631-205-4090
Email: pmenges[at]bio.uni-kl.de
Room: 24-101A

Project description:

Sara Bernhard - PhD Student

Tel.: +49 (0)631-205-5920
Fax: +49 (0)631-205-4090
Email: sbernhar[at]bio.uni-kl.de
Room: 24-109

Project description:

Cells often undergo tetraploidization during tumorigenesis. Tetraploid cells contain doubled chromosome and centrosome number and are inherently instable. Therefore, tetraploidy is considered to be an intermediate state leading from diploidy to aneuploidy. Proliferation of tetraploid cells is prevented by several molecular mechanisms, but some cells can escape and further proliferate, which then in turn facilitates tumor formation. My work focuses on the molecular mechanisms that allow tetraploid cells to escape the cell cycle arrest and apoptosis. 

Angela Wieland - PhD Student

Tel.: +49 (0)631-205-5919
Fax: +49 (0)631-205-4090
Email:
Room: 24-101A

 
Project description:

Narendra Chunduri - PhD Student

Tel. +49 (0)631-205-5920
Fax: +49 (0)631-205-4090
Email: chunduri[at]bio.uni-kl.de
Room: 24-109

Project description:

Every time the cell divides, all chromosomes have to be duplicated and segregated equally into the two daughter cells. When there are errors in segregation, the daughter cells will either lose or gain a chromosome. The propagation of these cells is usually limited by activation of the p53 pathway. However, the mechanisms underlying the p53 activation remain unclear. Using aneuploid cells (monosomic and trisomic) as a model system, I will investigate the mechanisms of p53 activation and the impact of p53 on the cellular response to aneuploidy.

Kristina Keuper - PhD Student

Tel.:+49 (0)631-205-5920
Fax: +49 (0)631-205-4090
Email:
Room: 24-109

Project description:

Sushweta Sen - PhD Student

Tel. +49 (0)631-205-5920
Fax: +49 (0)631-205-4090
Email: ssen[at]bio.uni-kl.de
Raum: 24-101A

Project description:

DNA replication and repair are essential processes which ensure efficient and accurate transfer of genetic material to the daughter cells. Failure in DNA replication or repair leads to various diseases including cancer, ageing or developmental disorders. In my project I’m studying the role of the SMC5/6 complex in DNA repair and in the structural maintenance of chromosomes. Using a cell-free system based on Xenopus laevis egg extracts I’m addressing how SMC5/6 is recruited to chromosomes and how it contributes to the repair of different DNA lesions.

Erna Dilger

Tel. +49 (0)631-205-4269
Fax +49 (0)631-205-4090
Email: edilger[at]rhrk.uni-kl.de
Room: 24-138

Isabell Kirchner

Tel. +49 (0)631-205-5921
Fax +49 (0)631-205-4090
Email:isabell.kirchner[at]bio.uni-kl.de
Room: 24-107

Robin Roth

Tel. +49 (0)631-205-5921
Fax +49 (0)631-205-4090
Email:rroth[at]rhrk.uni-kl.de
Room: 24-107