Research Groups

General Contact Information

Max Planck Institute
of Molecular Cell Biology and Genetics
- Grapin-Botton -

Pfotenhauerstr. 108
01307 Dresden

Current Lab Members

Name Position Email Phone
Beydag-Tasöz, Belin Selcen Predoc
Dietze, Sophia Apprentice Biologielaborant
Flasse, Lydie Postdoc
Franz, Antje Assistant to Anne Grapin-Botton +49 351 210-2730
Grapin-Botton, Anne Director +49 351 210-2500
Katsumoto, Keiichi Staff Scientist +49 351 210-2672
Kim, Yung Hae Staff Scientist +49 351 210-2671
Lee, Byung Ho Postdoc +49 351 210-2983
Petzold, Heike Technician +49 351 210-2743
Schewin, Coline Predoc +49 351 210-2676
Seijo Barandiaran, Irene Postdoc +49 351 210-2984
Stratmann, Johannes Postdoc +49 351 210-2981

Lydie Flasse

I am investigating how the planar polarity pathway can organize pancreatic progenitors in the complex network of tubes composing the pancreas. A better understanding of pancreatic epithelium architecture and how it influences cell fate choices will provide new insights into disorders associated with cyst formation and diabetes.

Keiichi Katsumoto
Staff Scientist

I study β-cell proliferation and β-cell maturation mechanisms. Diabetes is caused by many factors, but basically, diabetes patients have a problem in producing Insulin to control blood glucose level, which can involve decreased β-cell number and impaired β-cell function. If we can control β-cell proliferation and β-cell maturation in their body, we hope to overcome diabetes. I more specifically study Wnt signaling in these steps.

Yung Hae Kim
Staff Scientist

I'm working on differentiation dynamics of pancreatic progenitors to endocrine lineage during pancreas development by observing pancreatic progenitors' behaviors at single-cell resolution from mouse embryonic pancreas and human pluripotent stem cell (hPSC)-derived pancreatic cells. I use 2-D and 3-D live imaging, lineage tracing, single-cell transcription analysis, hPSC differentiation, and hPSC-derived pancreatic organoids. I'm also collaborating with mathematicians/physicists to model our data and test the model experimentally. The ultimate goal is to be able to control progenitor expansion and/or endocrine differentiation to boost production of beta-cells in vitro as a mean of beta-cell replacement therapy for type 1 diabetes.

Byung Ho Lee

Byung Ho is studying the influence of biophysical stimuli on the growing pancreas and pancreatic organoids. He is particularly interested in how mechanical deformations influence branching and differentiation of the pancreas and pancreatic organoids.

Heike Petzold

In addition to tasks related to laboratory organization, I work on the topic of apico- basal cell polarity in 3D pancreas organoid cultures.

Coline Schewin

It was recently shown in our lab that during development, the early secretion of fluid in the pancreas likely shapes the structure of the ductal network that deliver enzymes digesting food from their production site, in acini, to the intestine (Dahl-Jensen et al., 2018). In my project I study the influence of exocrine secretion flow on the morphogenesis of this ductal network. I am particularly interested in how the flow is generated, how it is sensed and its influence on the remodeling of the ducts.

Irene Seijo

I am studying planar cell polarity during pancreas development. I am particularly interested in understanding how tissue asymmetry is established and to analyze its role on cell differentiation.

Johannes Stratmann

Both, pancreas and nervous system contain highly specified cell types with shared secretory activities but distinct physiological functions i.e. metabolism vs. signal transduction. Intriguingly, many genes are shared across the two tissues. During my project, I intend to molecularly decode the conservation of gene regulatory networks (GRNs) of transcription factors, crucial for pancreas and spinal cord development. In addition, I aim to dissect the conservation of gene regulatory regions for key genes, controlling spatio-temporal gene expression. This will provide a regulatory map to help understand disease-causing mutations in non-coding regions controlling appropriate cell biogenesis in development.