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Fig. 8. Dominant-negative forms of RhoA and Rac1 block the overexpression effects of XLPA₂. (A) Low-power magnification. Scale bar: 20 µm. (Left panels) A control cap (upper) and a cap injected with 100 pg of XLPA₂ mRNA (lower) into each cell at the two-cell stage. (Upper middle) Overexpression of RhoA-N19 blocks purse-string formation and delays wound healing with no change on cortical actin. (Lower middle) The overexpression effects of XLPA₂ on wound healing are blocked by RhoA-N19, but not the increase in cortical actin. (Right panels) Rac-N17 also prevents purse-string assembly and reduces the amount of cortical actin (upper) and blocks the effects of XLPA₂ (lower). (B) High-power magnification. Scale bar: 5 µm. (Upper left) Cellular network in a cap injected with a low dose of XLPA₂ mRNA. (Lower left) Injection of RhoA-N19 results in an increase in cellular processes and (upper middle) prevents the formation of an actin purse-string (arrow). (Upper right) Cells in caps injected with both XLPA₂ and RhoA-N19 still have cell processes similar to RhoA-N19 alone and no purse-string. (Lower middle) Rac-N17 caused a decrease in the amount of cortical actin, decreased the number of cell processes, and caused the cells to become rounded. (Lower right) When co-injected with XLPA₂, Rac-N17 blocks the increases in cortical actin and formation of rigid network, but cell processes are still evident.

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