Modulation of chromatin organization by SUMO pathway in myofibril assembly and muscle atrophy
Research focus / Forschungsschwerpunkte
Mobility is an indispensable feature that determines survival and success in the animal world. Skeletal muscle that allows this mobility accounts for 40% of human body mass. Apart from movement, another feature of the muscle power is to be able to bear the load. The skeletal muscle displaying a characteristic striated pattern is an array of linearly arranged units called ‘sarcomeres’. The individual sarcomere hosts highly organized structures including the actin, and myosin filaments. The cyclic interaction between these two types of filaments is responsible for generation of force and movement at the molecular to organismic level.
Precise molecular arrangement of sarcomere is central to the muscle function. Importantly, disorganization of sarcomere and thereby defective muscle function are the typical hallmarks of myopathies including cancer cachexia, prevalent in nearly 80% of patients.
Our group aims to understand how SUMO (Small Ubiquitin-like Modifier)-mediated epigenetic program regulates sarcomere organization and how it is deregulated in muscle atrophy/cachexia.
- Modulation of chromatin organization by SUMO pathway in myofibril assembly.
- Epigenetic signaling in muscle atrophic condition/Cachexia.
Lab stuff / Labor Mitarbeiter
PhD student: We are currently hiring talented doctoral students.
Stefanie Nedel: technical assistant
With her excellent technical expertise in cell and molecular biology Stefanie is involved in various projects of the group.
We employ various experimental approaches including quantitative proteomics, epigenomics (ChIPseq, chromosome conformation capture etc.) and single molecule biophysical methods such as total internal reflection fluorescence microscopy (TIRFM) to address our questions.
Our lab is funded by research grant from the German Research Foundation (DFG).
Veröffentlichungen /Selected publications
- Nayak A*, Lopez-Davila AJ, Kefalakes E, Holler T, Kraft T, Amrute-Nayak M. (2019). Regulation of SETD7 Methyltransferase by SENP3 is Crucial for Sarcomere Organization and Cachexia. Cell Reports. Vol 27, issue 9, P2725-2736.e4, May 28. (*corresponding author)
- Amrute-Nayak M, Nayak A, Steffen W, Tsiavaliaris G, Scholz T, Brenner B. (2019). Transformation of Conventional, Non-processive Myosin II into a Fast Processive Motor. (2019). Small. Feb;15(7)
- Nayak, A*., Reck, A., Morsczeck, C., and Muller, S. (2017). Flightless-I governs cell fate by recruiting the SUMO isopeptidase SENP3 to distinct HOX genes. Epigenetics Chromatin .10, 15. (* corresponding author)
- Jung, J., Nayak, A., Schaeffer, V., Starzetz, T., Kirsch, A.K., Muller, S., Dikic, I., Mittelbronn, M., and Behrends, C. (2017). Multiplex image-based autophagy RNAi screening identifies SMCR8 as ULK1 kinase activity and gene expression regulator. Elife 6
- Nayak, A., Viale-Bouroncle, S., Morsczeck, C., and Muller, S. (2014). The SUMO-specific isopeptidase SENP3 regulates MLL1/MLL2 methyltransferase complexes and controls osteogenic differentiation. Mol Cell 55, 47-58
- Nayak, A., Glockner-Pagel, J., Vaeth, M., Schumann, J.E., Buttmann, M., Bopp, T., Schmitt, E., Serfling, E., and Berberich-Siebelt, F. (2009). Sumoylation of the transcription factor NFATc1 leads to its subnuclear relocalization and interleukin-2 repression by histone deacetylase. J Biol Chem 284, 10935-10946.
- Nayak, A., and Muller, S. (2014). SUMO-specific proteases/isopeptidases: SENPs and beyond. Genome Biol 15, 422.
- Dr. Chiara Luanzolo
Institute of Biomedical Technologies (ITB)-CNR
Chromatin and Nuclear architecture Laboratory
at Istituto Nazionale di Genetica Molecolare "Romeo ed Enrica Invernizzi” Milan, Italy
- Prof. Dr. med. Susanne Petri
Department of Neurology, Hannover Medical School, Carl-Neuberg-Str. 1, 30625 Hannover, Germany
- Prof. Dr. Christian Morsczeck
Department of Oral and Maxillofacial Surgery, University Hospital Regensburg, Germany