PhD student (f/m/x) in Köln

• Breeding of genetically modified mice
• Immunohistochemistry
• Isolation of single cardiac myocytes by laser dissection microscopy
• Flow cytometry
• Determination of single cell transcriptomes (collaboration with Cologne Center of Genomics, CCG)

• M.Sc. or equivalent degree in biochemistry, biology or a related field, completed with above-average grades
• Experience and a publication record in one of these fields
• Experience in mitochondrial biology would be an advantage
• High level of motivation, endurance and positivity
• Ability and willingness to work in a collaborative team
• Appreciation of thorough and dependable experimentation
• Excellent communication in English (written and spoken) 

Desired qualifications:

• Experience in immunohistochemistry
• Experience in mouse breeding 

• We are offering a highly motivated environment and access to all state of the art equipment in our central facilities.

As a modern maximum-care hospital with a capacity of approximately 1,540 beds, the University Hospital of Cologne is dedicated to the practice of innovative academic medical excellence. At the Faculty of Medicine 1.800 scientists are engaged in research, ranging from basic sciences to clinical application, as well as teaching and health care. Together with the University Hospital Cologne the faculty maintains 58 clinics, research institutes and centres. 3.400 students study in this dynamic and innovative environment. The Faculty of Medicine and the University Hospital Cologne are embedded in the scientifically highly active Rhine region. They have strong contacts to and alliances with the surrounding universities and non-university research institutions guaranteeing scientific excellence in research and teaching.

In this project, we will study the effect of accumulating mitochondrial DNA mutations on heart function during aging. Using a newly developed mouse model, we have shown that the accumulation of such mutations in a stochastic manner in single cardiomyocytes, giving rise to a tissue mosaic with only one out of two hundred cells being severely affected, leads to severe cardiac arrhythmia in mice (Baris et al., Cell Metab 2015). In order to understand the pathomechanism leading to this ageing associated cardiac disease, we will now study

1. the interaction of defective cells with the surrounding tissue and
2. if acceleration or slowing down the rate of mutation accumulation accelerates or slows down the progression of the disease.

Please visit to learn more about the group’s interests and ongoing research.

You will work at a small but very successful working group with access to all state-of-the-art equipment at our central facilities (CECAD, CMMC, CCG).