“Lessons from worms help us understand kidney regeneration and ageing”

Prof. Dr. Bernhard Schermer

Since 2007, Bernhard Schermer has been the Head of the Nephrolab Cologne. In 2001, he received his MD at the University of Frankfurt under the supervision of Prof. Rudi Busse, Department of Cardiovascular Physiology. As a research fellow at Harvard Medical School, Boston (MA), and as a post-doc at the University Hospital ­Freiburg, he focused on hereditary kidney diseases, signal transduction and the biology and function of primary cilia. In 2004, Schermer became independent junior group leader in the Benzing group at the University of Freiburg.

In 2007, both the Benzing and Schermer groups moved to the University Hospital Cologne where Schermer is now Assistant Professor at the Department of Medicine and Vice-Director of the Kidney Research Center Cologne. Also of note is that a number of his ongoing research projects are closely related to the Cologne Cluster of Excellence on Cellular Stress Responses in Ageing-Associated Diseases (CECAD).

Research interests

  • Function of primary cilia and the pathogenesis of “ciliopathies”
  • Glomerular filtration in the kidney and the pathogenesis of age-related kidney disease
  • VHL and longevity pathways in C.elegans and their role in kidney regeneration

Previous scientific achievements

In 2003, the Schermer group demonstrated that NPHP proteins, mutations in which cause a rare cystic kidney disease called Nephronophthisis (NPH), are localized in primary cilia – organelles that were regarded as evolutionary remnants for decades. Today, NPH and related diseases are regarded as “Ciliopathies”. In 2005, this group identified a phosphory­lation dependent mechanism regulating the ciliary trafficking of NPHP1 and the following year showed that the VHL ­tumour suppressor protein is required for ciliogenesis in mammals. Importantly, studies from 2009 revealed that loss of vhl-1 leads to a longevity phenotype in worms. In 2011, in collaboration with Prof. Bolz, the Schermer group identified and functionally characterized KIF7 as a novel ciliopathy gene causing Joubert Syndrome, and within the same year, discovered the first link between ciliary NPHP proteins and the Hippo signaling pathway, which is a master regulator of proliferation in the fruit fly Drosophila melanogaster.

Current projects

In close collaboration with other Sybacol groups, the Schermer group‘s overarching goal is to understand the signalling networks of ageing in model organisms and to transfer this knowledge to human aging and the pathogenesis of age-associated diseases. Therefore, this group studies mRNA and miRNA expression patterns and regulatory networks in genetic models with a phenotype of longevity or shortened lifespan. This research is mainly focused on the analysis of vhl-1 mutant worms. More specifically, in collaboration with Prof. Berg and Dr. Habermann, the Schermer group is working on tissue deconvolution of array results from biopsy material and analysing miRNA and mRNA networks in kidney development and age-related kidney disease,
respectively.

 

Selected Publications

Habbig, S., Bartram, M.P., Muller, R.U., Schwarz, R., Andriopoulos, N., Chen, S., Sagmuller, J.G., Hoehne, M., Burst, V., Liebau, M.C., Reinhardt, H.C., Benzing, T., and Schermer, B.: NPHP4, a cilia-associated protein, negatively regulates the Hippo pathway. J Cell Biol. (2011); 193(4): 633-642.

Benzing, T., and Schermer, B.: Transition zone proteins and cilia dynamics. Nat Genet. (2011); 43(8): 723-724.

Muller, R.U., Fabretti, F., Zank, S., Burst, V., Benzing, T., and Schermer, B.: The von Hippel Lindau tumor suppressor limits longevity.
J Am Soc Nephrol. (2009); 20(12): 2513-2517.

Schermer, B., Ghenoiu, C., Bartram, M., Muller, R.U., Kotsis, F., Hohne, M., Kuhn, W., Rapka, M., Nitschke, R., Zentgraf, H., Fliegauf, M., Omran, H., Walz, G., and Benzing, T.: The von Hippel-Lindau tumor suppressor protein controls ciliogenesis by orienting microtubule growth. J Cell Biol. (2006); 175(4): 547-554.

Schermer, B., Hopker, K., Omran, H., Ghenoiu, C., Fliegauf, M., Fekete, A., Horvath, J., Kottgen, M., Hackl, M., Zschiedrich, S., Huber, T.B., Kramer-Zucker, A., Zentgraf, H., Blaukat, A., Walz, G., and Benzing, T.: Phosphorylation by casein kinase 2 induces PACS-1 binding of nephrocystin and targeting to cilia. EMBO J. (2005); 24(24): 4415-4424.

Organisation / Institute
Department II of Internal Medicine
University Hospital Cologne

Address
Prof. Bernhard Schermer
Nephrolab Cologne
University Hospital Cologne
CECAD Research Center
Joseph-Stelzmann-Str. 26
50931 Köln, Germany

bernhard.schermer@uk-koeln.de

Loss of VHL leads to an increased lifespan in C. elegans. This effect occurs in the absence of daf-16, the downstream effector of the insulin pathway in C.elegans. Lower panel: The knockdown of daf-2, the insulin receptor of the worm leads to a nuclear localization of daf-16 due to impaired insulin signalling, whereas the knockdown of vhl-1 does not.