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FIGURE 8:. Model of how MgcRacGAP regulates active RhoA and Rac1 in dividing epithelial cells. Mgc's GAP activity is necessary to down-regulate the active population of RhoA at the division site and both RhoA and Rac1 at cell–cell junctions in epithelial cells, and failure to do so results in defects in cytokinesis and cell–cell junctions. Left, in dividing epithelial cells, Mgc is localized to the overlapping MTs of the spindle midzone, the equatorial cortex, and the apical surface of cell-cell junctions. Middle, in dividing control epithelial cells, active RhoA accumulates in a focused band at the cell equator, but in Mgc GAP-dead cells, equatorial RhoA activity is not focused. Both active RhoA and Rac1 accumulate at cell–cell junctions in control cells (indicated by stripes), but when Mgc's GAP activity is disrupted, Rac1-GTP is increased at bicellular and tricellular junctions, and RhoA-GTP coaccumulates with ectopic F-actin–rich junctional structures (indicated by stars). Right, Mgc's GAP activity is required for proper AJ structure. In Mgc GAP-dead cells, the intensity and apical polarity of AJs are disrupted. RhoA is known to regulate the apical actomyosin belt and AJ integrity. Expression of DN RhoA rescued the AJ defect in Mgc GAP-dead cells, suggesting that this defect was due to misregulated RhoA activity. In addition, RhoA and Rac1 can exhibit cross-talk to antagonize each other (indicated by double arrow). Image published in: Breznau EB et al. (2015) © 2015 Breznau et al. This image is reproduced with permission of the journal and the copyright holder. This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike license Larger Image Printer Friendly View

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