Dresden 2014 – scientific programme
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BP: Fachverband Biologische Physik
BP 10: Posters: Molecular Motors
BP 10.4: Poster
Tuesday, April 1, 2014, 09:30–12:30, P1
Bimodal transport in a system of active and inactive kinesin-1 motors — •Lara Scharrel1,2, Rui Ma3, Frank Jülicher3, and Stefan Diez1,2 — 1B CUBE - Center for Molecular Bioengineering, Technische Universität Dresden, Germany — 2Max Planck Institute of Cell Biology and Genetics, Dresden, Germany — 3Max Planck Institute for the Physics of Complex Systems, Dresden, Germany
Long-range directional transport in cells is facilitated by microtubule-based motor proteins. One example is transport in a neuron where groups of motor proteins, such as kinesin-1 and cytoplasmic dynein, ensure the supply and clearance of cellular material along the axon. Defects in axonal transport have been linked to Alzheimer and other neurodegenerative diseases. However, it is not known how in detail multi-motor transport is impaired if a fraction of motors is defective. To mimic impaired multi-motor transport in vitro, we performed gliding motility assays with varying fractions of active kinesin-1 and inactive kinesin-1 mutants. We found that impaired transport manifests in multiple motility modes: (i) a fast mode with gliding at single-molecule velocity, (ii) a slow mode with gliding at close-to zero velocity or stopping, and (iii) a mode with switches between fast and slow mode. Notably, the transition from fast to slow mode occurred at a threshold fraction of active motors. Furthermore, we developed a theoretical description which explains the bimodal motility as well as the sharp transitions between fast and slow motility. Our results demonstrate that, depending on the fraction of active motors, impaired multi-motor transport is either performed close to full speed or is out of action.