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. 2007 Feb 26;176(5):573–580. doi: 10.1083/jcb.200612043

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Copyright © 2007, The Rockefeller University Press

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Figure 2. — MIIA and IIB regulate protrusion and differentially control adhesion turnover. (A; top) Kymographs from control (pSUPER), MIIA-depleted (pSUP-IIA), and MIIB-depleted (pSUP-IIB) cells. (bottom) Overlay of periodicity and slope from the kymographs. (B) Protrusion rates from A. At least 12 cells (3–5 protrusions/cell) from four independent experiments were analyzed. Data is presented as the mean ± the SEM. (C) Image sequence of control (top; Video 7) and MIIA- (middle; Video 6) and MIIB-depleted cells (bottom; Video 8) cotransfected with paxillin-GFP. (D) Color-inverted image sequence of MIIA-depleted cell expressing paxillin-GFP (Video 9). Time is shown in seconds. (E) Image sequence of paxillin-GFP–expressing, MIIA- (top) or MIIB-depleted (bottom) cells cotransfected with mChe-MIIA or mChe-MIIB, respectively (not depicted). (F) Image sequence of paxillin-GFP–expressing, MIIA-depleted cell. Arrowheads point to central adhesions; arrows point to impaired disassembly at the trailing edge (Video 10). (G) Image sequence of paxillin-GFP in a MIIB-depleted cell (left) expressing mChe-IIA (not depicted) and a MIIA-depleted cell (right) expressing mChe-IIB (not depicted). Bars: (C) 5 μm; (D) 3 μm; (E) 5 μm; (F) 20 μm; (G) 5 μm. Videos 6–10 are available at http://www.jcb.org/cgi/content/full/jcb.200612043/DC1.