| dc.description.abstract | In Ustilago maydis hyphae, bidirectional transport of early endosomes
(EEs) occurs on microtubules (MTs) that have plus and minus ends.
The transport is powered by kinesin-3 towards the plus ends of MTs and
dynein towards the minus ends. Experiments show an accumulation of
dynein at the MT plus end.
To investigate the mechanism of this accumulation, I consider two extended asymmetric simple exclusion principle (ASEP) models for the
bidirectional transport of dynein in this thesis. In the simpler two-lane
model, collision between opposite-directed motors is excluded whereas
the more sophisticated 13-lane model takes into account that the MT
usually consists of thirteen protofilaments. The presence of multi protofilaments allows dynein to avoid collision with kinesin by changing protofilaments, a behaviour that has been experimentally described. Both models are supplied by quantitative data obtained in U. maydis by live cell
imaging and suggest that the stochastic behaviour of dynein can account
for half of dynein motors in the accumulation at the MT plus end. Moreover, for the two-lane model, by using a mean field approximation, I give
an analytical approximation for the accumulation size which shows linear dependence on the flux. In contrast, this dependence is nonlinear in
the 13-lane model and appears to be associated with a phase transition
leading to a "pulsing state".
Accompanied experimental studies have shown that U. maydis contains
a complex MT array and that kinesin-3 moves early endosomes along
antipolar MT bundles. In order to better understand the bidirectional
EE motility, I extend the two-lane ASEP to model bidirectional transport
along an antipolar MT bundle. In this model, the MTs are coupled at
minus ends where organelles can switch MTs on which they move. By a
mean-field approximation and numerical simulations, I investigate how
the switching affects phases of density profiles as well as the type of
motor that dominates the active transport in the bundle. | en_GB |
