| Kris Girard
Uncovering the underlying mechanisms of cytokinesis
My research focuses on understanding the fundamental mechanisms that control how cells change shape during cytokinesis. Cortical viscoelasticity, along with cytoplasmic viscoelasticity and force production, modulate these stereotypical shape changes. I have been concentrating on uncovering the effect of the motor protein, myosin-II, and two actin cross-linking proteins, dynacortin and cortexillin-I, on these dynamic cell elements.
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Myosin-II localizes to the cleavage furrow during cytokinesis and is believed to be the major generator of force. Removing myosin-II from cells causes a cytokinesis defect in suspension cultures and increases the overall cortical viscoelasticity of the cells. |
| GFP Myosin-II |
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GFP Cortexillin-I
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GFP Dynacortin
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Dynacortin and cortexillin-I have complementary distributions during cytokinesis: cortexillin-I is enriched in the cleavage furrow, dynacortin is almost entirely excluded, and instead distributes globally around the cortex of the cell. The loss of either protein affects Dictyostelium growth rates, morphology, and cortical viscoelasticity. |
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| I measure the cortical viscoelasticity of different Dictyostelium strains by a technique called laser tracking microrheology (LTM). A laser is used to track the Brownian motion of a bead attached to the extra-cellular surface of the cell. The bead deflects the laser far-field as it moves. The new position is tracked by a quadrant photo-diode detector. From a plot of the tracking, a mean square displacement is calculated. The MSD is proportional to the cortical viscoelasticity. The smaller the MSD, the stiffer (or more viscoelastic) the cell is. |
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| Interestingly, the research has indicated that it is the mechanical properties that are the critical components governing cytokinesis rather than specific biochemical activities used to generate these properties. |