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We subsequently examined the lamellar dynamics of myosin II mutant hemocytes during collisions.
To assess whether the actin fiber formed in zip 1 and dia 5 mutant hemocytes during collisions, an 8.1 by 11.7 μm region within the lamella perpendicular to the site of initial cell contact was manually cropped from each colliding partner.
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As dia 5 mutant hemocytes showed uncoordinated cytoskeletal dynamics during collisions, we wanted to determine whether this defect also led to an uncoordinated kinematic response during CIL.
We next determined how the alteration in cell repulsion in dia 5 mutant hemocytes affected their ability to form an evenly spaced pattern during their developmental dispersal.
For analysis on the internuclear distance and nuclear speed during collisions n = 20 for both control and dia 5 mutant hemocytes.
Similarly to SCAR Δ37 mutants, Hem mutant hemocytes became highly vacuolated.
Left: diaphanous mutant hemocytes containing labeled F-actin undergoing a collision.
For this analysis only SCAR Δ37 mutant hemocytes with large lamellipodia were quantified.
These data suggest that dia 5 mutant hemocytes fail to actively repel each other.
Left: myosin II mutant hemocytes containing labeled F-actin undergoing a collision.
Spreading hemocytes on a cleaned glass slide, we observed that the cell areas of adherent eater mutant hemocytes were small compared to those of control w hemocytes (Fig. 3D).
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