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Professor Mathias Gautel MD PhD

BHF Professor of Molecular Cardiology

MGautelMathias2_140x180uscle Cell Biology
New Hunt's House
Guy's Hospital
London SE1 1UL
Email: mathias.gautel@kcl.ac.uk

PA: Gabriele Wright 
Email: gabriele.a.wright@kcl.ac.uk 

Biography

Professor Gautel received his MD from Heidelberg University in 1991, and was then a post-doctoral fellow and visiting team leader (1996-1998) at EMBL Heidelberg, where he worked on his habilitation (MD PhD equivalent) in Biochemistry on titin-based sarcomere assembly at Heidelberg University in 1998. After nine years at EMBL, Professor Gautel was awarded a Heisenberg Fellowship by the German Research Foundation, and joined the Max-Planck-Institute of Molecular Physiology, Dortmund, as a group leader. He was appointed as Professor of Molecular Cardiology at King’s College London in 2002, and was awarded the British Heart Foundation Chair of Molecular Cardiology at King’s in 2008. He heads the Randall Muscle Signalling and Development Section, and the KCL BHF Centre of Research Excellence Muscle Cell Biology theme.  He is European Coordinator of the Fondation Leducq Translatlantic Network of Excellence "Proteotoxicity: an unappreciated mechanism of heart disease and its potential for novel therapeutics"

Professor Gautel was awarded the International Society for Heart Research (ISHR) Outstanding Investigator Award in 2009. He was elected as a Fellow of the Academy of Medical Sciences (FMedSci) in 2010.

The laboratory uses molecular genetic, cell biophysical and biophysical, biochemical, structural, and physiological methods to study the biological principles that underpin sarcomere assembly, signaling, and controlled proteolytic turnover. Current areas of interest include mechanosignalling by muscle cytoskeletal proteins, their cross-talk with the proteolytic systems of muscle and gene expression regulation, and the perturbation of these processes in acquired and inherited muscle diseases.


Research Interests

We are interested in the communicational and structural network formed by the contractile machinery of muscle, and how this is assembled and turned over. Voluntary movement of our body, and the pumping functions of the heart require the actions of striated muscles, so called because of their extremely regular striation pattern visible when viewed under the microscope. These stripes are repetitive arrangements of molecular machines, called sarcomeres that generate force and movement. While muscle is mechanically active, its communication functions are also mechanically modulated.

Our research is centred on the mechanisms that organize, regulate, and remodel the sarcomere, and how sarcomeres crosstalk to mechanisms controlling muscle growth or atrophy. Genetic or acquired muscle diseases can disrupt this interplay of form and function. We are investigating how these disruptions of muscle signalling work on the molecular level.

Sarcomeres are complex macromolecular assemblies, built of many self-interacting proteins that are organised in a highly specific way into filamentous and anchoring structures. In the sarcomere, three systems of molecular filaments are involved in this assembly: actin filaments, which are held together at the Z-disk, myosin filaments, held together at the M-band, and the giant protein filament titin, which links the actin and myosin filaments.

Muscle responds rapidly to changes in use, with disuse leading to muscle loss (called atrophy) and exercise leading to muscle growth (called hypertrophy). These processes need to be constantly balanced, and to be linked to those controlling muscle repair. Signals controlling muscle growth, atrophy and repair signals originate at the M-band and the Z-disk. These structures contain proteins that can sense mechanical strain, the most important factor controlling muscle growth and atrophy. Our studies investigate the role of mechanosensors, and why mutations in some of the proteins (like the giant protein titin) can lead to muscle disease.

However, many of the proteins that we have recently discovered are also expressed in smooth muscle cells and other cell types of the cardiopulmonary system, where they may be similarly involved in coordinating mechanosignals with pathways that control functional plasticity by regulated protein turnover and transcriptional regulation. Striated muscle may thus serve as a paradigm for mechanosignalling in many cell types. Future work will therefore increasingly translate these observations to mechanosignalling in other contractile cells of the cardiovascular-pulmonary system, using biophysical and cell biophysical, genetic and biochemical approaches.

Group Members

Molecular Cardiology and Muscle Cell Biology Staff
  • Alexander Alexandrovitch, PhD (Postdoctoral Fellow)
  • Birgit Brandmeier (Senior Research Assistant)
  • Atsushi Fukuzawa, PhD (Postdoctoral Fellow)
  • Andrea Ghisleni (Early Stage Researcher)
  • Mark Holt, PhD (Senior Research Fellow)
  • Ay Lin Kho, PhD (Postdoctoral Fellow)
  • Martin Rees, PhD (Postdoctoral Fellow)
  • Katharina Jenniches (Research Associate)
  • Eva Masiero, PhD (Postdoctoral Fellow) 
PhD students
  • Ms Jessica Stuart 
  • Mr Luke Smith
  • Ms Roksana Nikoopour 

visit the king's research portalfor mathias gautel's publications
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