Mathematics Colloquia and Seminars
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Modeling and Simulation of Cytokinesis Ring ConstrictionMathematical Biology
|Speaker: ||Dietmar Oelz, UC Davis|
|Location: ||2112 MSB|
|Start time: ||Mon, Mar 10 2014, 3:10PM|
The aim of this work is to gain understanding of how the inner components
of certain non-muscle actomyosin bundles, specifically cytokinesis
constriction rings, but also stress fibers and the keratocyte rear bundle,
interact in order to effectuate contraction.
It is generally accepted that the force generated by myosin-II thick
filaments interspersed within the disordered ring-shaped bundle of
actin filaments largely contributes to the observed contraction. Yet,
randomly placed myosin-II is expected to contract or to expand its
vicinity with equal probability. Hence some sort of asymmetry which favors
contraction is usually stipulated.
Typically existing studies suggest that local asymmetry is provided by
either actin or myosin patterning, or by an involved mechanism which
favors contraction. Alternatively it is also suggested that actin
depolymerization provides contractile force.
Our approach is to formulate a detailed microscopic ODE-model for the
dynamics of a network of cross-linked actin filaments interspersed with
myosin-II motor proteins and to come up with a minimum set of modeling
assumptions which allow to simulate the observed ring constriction.
The result of our numerical experiments is that a disordered bundle of
actin filaments tends to contract if the positioning of myosin-II binding
sites has a bias towards the pointed ends of actin filaments. Furthermore
we found based on simulations that actin treadmilling in combination with
actin cross-linking has the potential to provide this kind of bias thus
allowing myosin-II to effectively contract the cytokinesis ring.